Kidney And Ureter Renal Cell Carcinoma Neoplasms Perinephric Abscess Notes

Kidney And Ureter

Surgical Anatomy Of Kidney

• Kidneys are bean-shaped retroperitoneal organs placed one each on either side of the vertebral column. Kidneys are often referred to as reniform (kidneylike), implying no parallels in their contour. Owing to the presence of the liver, the right kidney is 1–2 cm lower than the left kidney. The right kidney extends from L1 to L3, and the left kidney extends from T12 to L3.
• Anatomical relations of the kidneys are important, as they may get injured during kidney operations and may get directly involved by the local spread of renal malignancies.

Read And Learn More: Surgery of Urology Notes

Relations of kidneys:

Fascial Attachments:

The kidneys and ipsilateral adrenal glands are tightly wrapped by a fibrous capsule (perirenal fat and the Gerota’s fascia). Both these covers can be surgically lifted off the kidneys. This cover has a distinct yellowish brown hue which helps distinguish it from peritoneal fat, which is yellow in colour.

• Perinephric fat and the renal pedicle are responsible for the classical ballotability of renal swellings.
• The kidneys possess intrinsic anteroposterior mobility as they are suspended from the great vessels upon their pedicles and held in position within pliant perinephric fat contained within the anterior and posterior sheaths (laminae) of the Gerota’s fascia (renal fascia). This anatomical feature is responsible for the classical clinical sign of ballotability (Italian word that means tossing a ball) of renal swellings.

Superiorly:

The anterior and posterior sheaths of the Gerota’s fascia fuse at the superior limits of the adrenal gland only to blend further with the intrinsic fascia of the diaphragm. This anatomical arrangement allows the kidneys, which are retroperitoneal, to move with respiration (which is otherwise a feature of intraperitoneal structures).

Medially:

The anterior sheath or lamina (also called fascia of Toldt) blends with its counterpart from the other side anterior to the aortThe inferior vena cava is closely related to the overlying peritoneum, while the posterior sheath or lamina (also called fascia of Zuckerkandl) gets attached to the ventral surface of the vertebral bodies.

Inferiorly:

Gerota’s fascia remains an open potential space that contains the ureter and gonadal vessels.

Gerota’s fascia forms an important anatomical barrier and tends to confine pathological processes that originate from the kidney.

However, because of its deficiency inferiorly, a collection within Gerota’s fascia may track down and extend into the pelvis.

Some Points to Remember:

• The entire renal arterial system comprises end arteries (without anastomosis and collateral circulation). Occlusion of any branches of the renal artery within the kidney (known as segmental arteries) results in infarction of the area supplied by it.
• In contrast, the renal parenchymal veins anastomose freely with each other and the perinephric veins.

Polycystic Kidneys (Congenital Cystic Kidneys)

Congenital cystic disease of the kidneys is broadly of two types—genetic and non-genetic.

Two entities under the genetic type are important— autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD).

Examples of non-genetic cystic lesions are multicystic dysplastic kidney and multilocular cystic nephrom

Polycystic Kidneys Types:

• ADPKD: Autosomal Dominant Polycystic Kidney Disease.
• ARPKD: Autosomal Recessive Polycystic Kidney Disease.

Autosomal Dominant Polycystic Kidney Disease (ADPKD):

• It is the most common inherited cystic disease of the kidneys with an incidence of 1 in 1000.
• Both sexes are equally affected.
• It typically presents in adulthood, but earlier presentation may occur.

Associated Lesions:

• Cysts of the liver (most common—33%)
• Berry aneurysms (30%)
• Cysts of the pancreas (10%)
• Cysts of the spleen (<5%)
• Mitral valve prolapse
• Cysts in the seminal vesicles (30%)
• Cysts in the testis and prostate (extremely rare)
• Ovarian cysts

Polycystic Kidneys Pathology:

During development, some of the uriniferous tubules fail to join with the collecting ducts and develop into cysts. PKD1 gene on chromosome 16 and PKD2 gene on chromosome 4 are the culprit genes.

The important pathological features are as follows:

• Both kidneys are affected.
• They often enlarge to 3–4 times the normal size.
• Cysts are distributed evenly throughout the cortex and medulla.
• The contents of the cysts vary but do not contain urine.
• The kidneys are studded with multiple large cysts.
• When a cyst ruptures into the pelvis of the kidney, it results in haematuria.
• As the disease progresses, cysts progress in size, leading to pressure atrophy of the functional renal parenchyma and renal failure.

Polycystic Kidneys Clinical Features:

• Even though it is congenital, it manifests around 40 years of age.
• Dull-aching (dragging) pain in both loins is due to stretching of the renal capsule.
• Microscopic or macroscopic haematuria occurs in 70–80% cases.
• Secondary hypertension (75%) is due to renal ischaemia, which stimulates the juxtaglomerular apparatus to secrete renin. It may also be related to a separate genetic factor.
• Bilateral renal mass: Both kidneys are enlarged, have a nodular or bosselated surface, are firm to hard consistency, and are sometimes cysti
• Features of renal failure: Thirst, vomiting, abdominal distension due to paralytic ileus, anuria, uraemic smell, coated tongue, and anaemiRenal failure is the most common cause of death.
• Infection, pyelonephritis.
• Acute pain occurs if there is haemorrhage into or infection of a cyst. Colicky pain is due to a blood clot in the ureter.

Polycystic Kidneys Diagnosis:

1. Serum urea and creatinine to rule out renal failure. Normal creatinine levels: 0.8–1.6 mg%. Normal urea: 20–40 mg%.
2. Abdominal USG/CT scan to confirm the diagnosis.
3. IVU: Spider leg deformity of the calyces (Swiss cheese appearance).

Polycystic Kidneys Treatment:

• The asymptomatic polycystic kidney does not require any treatment other than regular follow-up.
• Polycystic kidney with hypertension: Control hypertension with drugs. If hypertension is uncontrollable, bilateral nephrectomy followed by renal transplantation is done.
• Infected cyst or if pyelonephritis develops: Appropriate antibiotics are given, and if necessary, the cyst is aspirated under ultrasound guidance.
• Polycystic disease with renal failure: Emergency dialysis followed by renal transplantation is the treatment of choice. The related donor should be screened for polycystic trait.

Autosomal Recessive Polycystic Kidneys:

This occurs in 1 in 10,000–40,000 cases and presents during infancy or childhood (hence, referred to as ‘infantile polycystic kidneys’). Oligohydramnios with large echogenic foetal kidneys on prenatal ultrasound suggest a more severe form of this disorder. Large renal masses may cause obstructed labour and neonatal mortality. Those diagnosed in the neonatal period, infancy, or early childhood have a poor course due to immature lungs and congenital hepatic fibrosis, which are invariable associations of this disorder. These children may also have facial and limb abnormalities. Almost all succumb to fatal uraemia and portal hypertension. Very few reach adulthood and become candidates for renal transplantation. There is no cure for this condition. Only palliative treatment can be offered.

Horseshoe Kidney

It is the most common renal fusion abnormality. Prior to the 6th week of intrauterine life, the metanephric blastema, which are bilateral structures that give rise to the definitive kidneys, are very close to one another in the pelvis. If the caudal ends of these fuse in the midline around this time (Theory: Overcrowding in the pelvis by large umbilical arteries), normal rotation and ascent is prevented, resulting in horseshoe kidney—the most common fusion anomaly.

• Rarely, upper polar fusion may occur, giving rise to reverse horseshoe kidney.
• The inferior mesenteric artery crosses the isthmus at the level of L3–L4. Hence, the horseshoe kidney cannot ascend fully. It is felt lower down in the abdomen. Associated anomalies.

Horseshoe Kidney Clinical Features:

• Horseshoe kidney occurs once in 500 live births with a male preponderance (M : F—2 : 1).
• It may be asymptomatic for many years.
• A palpable mass below and to the right and left of the umbilicus or umbilical region may be a horseshoe kidney.
• Recurrent urinary tract infection (UTI) is common because the ureters are angulated over the kidney isthmus.
• They are more prone to hydronephrosis due to angulation of the ureters.
• Rovsing’s sign: Hyperextension of the spine results in abdominal pain, nausea, or vomiting due to stretching of the capsule.

Horseshoe Kidney Diagnosis:

• Ultrasonography (USG) to locate the kidney.
• IVU: Upper and middle calyx are directed laterally but the lower calyx is directed medially where there is fusion, which is characteristic of horseshoe kidney.
• CT scan or isotope renogram are confirmatory.

Horseshoe Kidney Treatment:

• Indicated only when there are complications.
• Removal of the stone or repair and reconstruction of hydronephrosis are done in a standard manner.
• For aortic aneurysm repairs, the isthmus may need to be divide

Renal Stones

Aetiopathogenesis:

Lithogenesis involves complex physical–chemical interactions in vivo. These are summarized as follows:

1. Infection: Organisms such as Proteus, Pseudomonas, and Klebsiella produce recurrent UTI. These organisms produce the enzyme urease, which splits urea into ammonium and carbon dioxide. Ammonium renders the urine alkaline, which facilitates the precipitation of phosphates. Triple phosphate stones (also called struvite stones) are formed in this manner. The nucleus of the stone may harbour these bacteria.

2. Hot climate causes dehydration, which results in the production of highly concentrated urine laden with precipitable solutes, namely calcium and oxalate, which lead to the formation of calcium oxalate stones.

3. Dietary factors:

• Diets rich in red meat, fish, and eggs may give rise to aciduria (purine-rich diet causes uric acid stones).
• Diets rich in calcium—tomatoes, milk, spinach, rhubarb—produce calcium oxalate stones.
• Diets lacking vitamin A cause desquamation of the urothelium and cellular debris, providing a nidus for crystal aggregation around it.

4. Metabolic causes:

• Hyperparathyroidism increases serum calcium levels by parathormone-induced hypercalciuria which complexes with oxalate crystals to form renal stones.
• Gout increases uric acid levels and causes multiple uric acid stones. Any cause of hyperuricaemia (increased uric acid levels in the serum) can cause aggregation of uric acid crystals to form uric acid stones. Common causes of hyperuricaemia include dietary excess, gout, and increased cellular destruction as in chemotherapy.

5. Immobilisation: Immobilisation, as in bedridden patients, leads to extensive bone demineralization. This in turn causes hypercalciuria, which increases the risk of stone formation. Such stones are called “recumbency stones.”

6. Decreased urinary citrate: Citric acid (300–900 mg/ 24 hours) keeps the urinary pH low. When citric acid levels decrease, it promotes the precipitation of urinary calcium. Citrate excretion is under hormonal control. Citrate is a naturally occurring stone-inhibiting substance.

7. Urinary stasis: Urinary stasis due to resistance to urinary flow (horseshoe kidney, ectopic kidneys, congenital pelvic ureteric junction obstruction, congenital vesicoureteric junction obstruction, etc.) increases the risk of infections and stone formation.

8. Randall’s plaques: Randall’s observation of submucosal whitish-yellow precipitations of crystalline substances at the tips of renal papillae—well-known as Randall’s plaques—supports the “fixed particle theory” of lithogenesis. The fixed plaque initiates nucleation, the first step in stone formation. Nucleation can be induced by a variety of substances—free crystals (free particle theory), proteinaceous matrix, foreign bodies (suture material), crystals in clogged lymphatics (Carr’s hypothesis), and particulate tissue.

Types of Renal Stones

1. Calcium Oxalate Stones:

• They are the most common variety (85%) of urinary calculi.
• Two subtypes: Relatively friable calcium oxalate dihydrate (Weddelite) and harder calcium oxalate monohydrate (Wewellite).
• They are radio opaque.
• They are called mulberry stones as they resemble the mulberry fruit.
• Their thorny surface can abrade the urothelium and cause haematuria, which in time imparts a brownish hue to these stones (acid hematin forms by the breakdown of haemoglobin in acidic urine).
• Small spiky stones cause intense pain, especially when they travel down the ureters.
• In infected urine, they exist as mixed stones (calcium oxalate and calcium phosphate).
• Citrate deficiency is often found in patients with this type of stone.

2. Uric Acid Stone:

• Comprise 5–10% of all stones
• Pure uric acid stones are radiolucent.
• Usually multiple with a smooth surface and yellowish hue.
• Acidic pH and dehydration favour their formation.
• May occur as a mixed stone with calcium oxalate, which is visible on X-ray KUB.
• Common in those who eat red meat.
• Amenable to medical management by alkalanization.
• Suitable for extracorporeal shockwave lithotripsy (ESWL).

Lesch-Nyhan syndrome is a rare inherited disorder, wherein high levels of uric acid production result in uric acid stones. High levels of uric acid in the blood can form needle-like crystals in a joint and cause episodes of severe and sudden pain, tenderness, redness, and swelling (gout).

3. Phosphate Stone:

• Pure calcium phosphate stones are rare and are more common in women than in men

 

• They usually occur as triple phosphate stones (calcium, magnesium, and ammonium—struvite).
• With growth, they tend to fill the collecting system and become its cast. Such configuration resembles the branched horn of a stag, hence called ‘staghorn calculus’.
• Alkaline urine facilitates their formation (infections due to urea-splitting bacteria typically render the urine alkaline, hence called infection stones).
• Infection stones may cause recurrent urinary tract infections and in the long run cause renal parenchymal damage.

4. Cystine Calculus:

• Cystinuria is an inborn error of metabolism that occurs due to decreased reabsorption of cystine from the renal tubules.
• Occurs in young girls at puberty.
• Increased excretion of cystine in the urine results in cystine calculus.
• Stones are hard and radio-opaque due to sulphur.
• Benzene/hexagonal crystals in the urine.
• D-penicillamine is administered to dissolve the stones.

Renal Stones Clinical Features:

• Renal pain: Dull-aching to pricking type of pain is present posteriorly in the renal angle formed by the sacrospinalis and the 12th riPain is the most common symptom and is not related to the size of the stone. Murphy’s kidney punch test demonstrates tenderness at the renal angle. The same pain may sometimes be felt anteriorly in the costal margin. Hence, it is described as costovertebral pain. Nausea and vomiting are due to intense sympathetic stimulation caused by stretching of the renal capsule mediated by the coeliac plexus.
• Ureteric colic: When the stone is impacted in the pelviureteric junction or anywhere in the ureter, it causes severe colicky pain originating in the loin and radiating to the groin, testicles, vulva, and medial side of the thigh. This may be associated with strangury. The referred pain is due to irritation of the genitofemoral, ilioinguinal, and iliohypogastric nerves.
• Haematuria is common with renal stones because the majority of stones are oxalate stones. The quantity of blood loss is small, but it is fresh blood (Key Box 57.2).
• Recurrent UTI: Fever with chills and rigors, burning micturition, pyuria, and increased frequency of micturition.
• Guarding and rigidity of the back and abdominal muscles during severe pain.

Renal Stones Complications:

1. Calculous hydronephrosis occurs due to back pressure producing renal enlargement. Stretching of the renal capsule results in pain. In such cases, an associated palpable kidney mass suggests hydronephrosis.
2.  Calculous pyonephrosis: Infected hydronephrosis wherein the kidney is converted into a bag of pus.
3. Renal failure: Bilateral staghorn calculi may not be symptomatic until they present with uraemia and renal failure.
4. Squamous cell carcinoma: Long-standing stones increase the risk of carcinoma.

Renal Stones Investigations:

1. Blood urea and creatinine to rule out renal failure.

2. Plain X-ray KUB:

• To diagnose stones. 90% of renal stones are radiopaque.
• An enlarged renal shadow can be seen.

3. USG:

• The presence of the stone can be confirmed.
• The exact size and location of the stone can be evaluated.

4. Noncontrast CT scan: It is the gold standard investigation.

5. Intravenous urogram (IVU)

• To accurately locate the stone within the collecting system of the kidney (pelvicalyceal system and ureter) and to assess renal function. A nonradiopaque stone can be seen as a filling defect. Hydronephrosis and hydronephroureterosis may be seen.
• CT scans are used to more accurately detect causes of abdominal colic.

6. Urine for culture and sensitivity.

7. Metabolic workup is done in young patients with stones, recurrent stones, nephrocalcinosis, and struvite stones—serum uric acid, ionized calcium, etc.

Renal Stones Treatment:

The treatment of renal stones can be divided into nonoperative treatment and operative treatment.

1. Nonoperative Treatment:

1. Conservative: Small stones < 5 mm in size and stones in the lower ureter may pass off with a copious amount of fluid intake and at times with forced diuresis. Intravenous hydration followed by intravenous frusemide may help to spontaneously pass the stones.

2. Extracorporeal shock wave lithotripsy (ESWL): It is indicated for stones <2 cm in size. It causes stone fragmentation by focusing externally generated shock waves on the stone within the renal collecting system through intact skin and across the body wall.

There are three methods of shock generation: Electromagnetic, piezoelectric, and electrohydrauli The lithotripters depend on either ultrasound or fluoroscopy for stone localization. ESWL is performed in situ when the stone burden is <1 cm and after cystoscopically placing a DJ stent for a larger stone burden because there may be obstructive columnation of stone fragments in the ureter. The fragments that result after ESWL are passed naturally.

Hard stones like cystine and calcium oxalate monohydrate are refractory to treatment by ESWL.

2. Operative Treatment

1. Endoscopic procedures
2. Open surgical procedures

1. Endoscopic Procedures:

Percutaneous nephrolithotomy (PCNL): It is indicated for stones > 2 cm in size. Retrograde pyelography (RGP) is done when the stone is located in the pelvis of the kidney. With a small 1 cm incision in the loin, the PCNL needle is passed into the pelvis of the kidney and confirmed by fluoroscopy. A guidewire is passed through the needle into the pelvis of the kidney. The needle is withdrawn, with the guidewire is left within the pelvis. Dilators are passed over the guidewire, and a working sheath is introduced into the pelvis. A nephroscope is passed into the pelvis, and if the stone is small, it can be removeIf it is big, it may have to be crushed using ultrasound probes, after which the fragments are removeUltrasound or pneumatic energy is used for fragmenting. Holmium-Yag laser may also be used to fragment the stones. Laser fiber may be introduced through the operating nephroscope to achieve this. The method of fragmenting renal stones using different energies introduced through endoscopes is called intracorporeal lithotripsy.

Complications of PCNL:

• Injury to the colon/sepsis
• Injury to the blood vessels
• Urinary leaks may persist for a few days.

2. Open Surgical Procedures:

Depending on the stone’s location, various procedures are done.

1. Pyelolithotomy: When there is extrarenal pelvis.
2. Nephrolithotomy: When there is intrarenal pelvis, the stone has to be removed by incising the kidney parenchyma.
3. Extended pyelolithotomy: By retracting the kidney parenchyma from the collecting system, the incision over the pelvis can be extended to the calyx to remove a stone present there. Even a large staghorn calculus can be removed.
4. Pyelonephrolithotomy: The stone is extracted through an incision in the pelvis and the renal parenchyma.
5. Partial nephrectomy: When the stone is impacted in polar calyces and causes segmental atrophy (polar scarring).
6. Nephrectomy: Significant functional loss (poorly functioning kidney) which is not expected to recover even after stone removal. This is done in patients with recurrent infections.

Special Situations:

Bilateral renal stones: Dealing with bilateral stone disease is a matter of clinical judgment. In most instances, the time interval between interventions for both sides is 1–2 weeks.

 

Hence, the symptomatic or obstructed side is dealt with first. If both kidneys are obstructed or are causing symptoms, any one side is destoned (rendered stone-free) in the first phase with concurrent drainage (DJ stenting or percutaneous nephrostomy) for the other side, which is dealt with after 1–2 weeks.

In bilateral disease, if the patient is uremic, urgent bilateral drainage either by DJ stenting or nephrostomy is performed

Definitive intervention is done once functional recovery takes place. Kidneys with better function should be operated first. The opposite side can be operated 1–2 weeks later.

If there is pyonephrosis with high-grade fever, pain, and tenderness, percutaneous nephrostomy is done under ultrasound guidance in which a tube drain is placed in the pelvis of the kidney to drain the pus and urine.

Once the pus clears, renal function is reassessed the kidney is nonfunctioning, and nephrectomy is done. If the kidney is functioning, ESWL/PCNL/open procedure is done.

Ureteric Stone

Stones come down from the pelvis of the kidney and may get impacted at any site of anatomical narrowing of the ureter, namely:

1. Pelviureteric junction
2. Crossing of the iliac artery
3. Crossing of the vas deferens or broad ligament
4. Site of entry into the bladder wall
5. Ureteric orifice

If left untreated, it may lead to hydroureteronephrosis, renal parenchymal atrophy, infection, and/or pyonephrosis.

Ureteric Stone Clinical Features:

• Pain in the loin radiating to the groin: Pain is severe, colicky, intolerable, and lasts for a few hours. When the stone descends into the lower ureter, pain radiates to the testicles, labia majora, and the upper portion of the thigh due to irritation of the genitofemoral nerve. Colic lasts for 4–6 hours and is relieved by antispasmodics, narcotics, and NSAIDs. This is the most common clinical presentation of ureteric stones.
• Microscopic haematuria invariably accompanies acute ureteric colics. Some patients have gross haematuriAt times, it may present with fever and chills, suggestive of UTI when pyuria is also present.
• Guarding and rigidity of the abdominal wall, if present on the right side, may be confused for acute appendicitis.

Ureteric Stone Investigations:

Same as for renal stone.

Ureteric Stone Treatment

1. Most ureteric stones pass naturally (urine). The patient is asked to consume a lot of water and take antispasmodics. Oral administration of alphablockers (example: Tamsulosin) with or without deflozacort may be used to achieve stone expulsion (medical expulsive therapy).
2. Flushing therapy: About 2 L of IV fluid, with 20–40 mg Inj. frusemide (Lasix). It may be repeated for a few days.
3. Stone in the upper ureter: ESWL is the ideal treatment. Retrograde intrarenal surgery (RIRS) is done for ureteric, renal, and calyceal stones. Flexible ureteroscopy with laser fragmentation may also be done.
4. Middle ureteric stone: ESWL, ureteroscopy basketing, or open surgery (ureterolithotomy).
5. Lower ureteric stone: Ureteroscopic removal. With the use of a ureteroscope, direct visualisation and manipulation of the stone (even if it is impacted) can be done. A laser or ultrasonic lithotripter can be used to disintegrate the stone.
6. Vesicoureteric junction: Ureteroscopic removal or endoscopic meatotomy of the vesicoureteric junction. For a stone impacted at the ureterovesical junction, cystoscopy is performeThe ureteric orifice is identified, and a cut is given at its mouth. Under fluoroscopic monitoring, the stone can be manipulated and basketed out using a dormia basket or other type of basket.
7. An impacted stone which is not amenable to ESWL, fluoroscopic, or ureteroscopic manipulation has to be extracted by ureterolithotomy (open surgical method).

Prevention of Stone Disease:

• Metabolic work-up of urine and blood to identify metabolic causes. Example: Hyperparathyroidism should be suspected when serum calcium is high. It should be followed up with a parathormone assay as a confirmatory test.
• Fluid management: 1.5 L/day
• Dietary adjustment: Red meat (rich in uric acid) to be avoided.
• Drug treatment
• Allopurinol, sodium bicarbonate: Uric acid stones
• Potassium citrate: Calcium stones
• Thiazides small dose: Calcium stones
• D-penicillamine: Cystine stones
• Urease inhibitors (e.g. acetohydroxamic acid): Infection stones.

Hydronephrosis

Hydronephrosis Definition:

Aseptic dilatation of the pelvicalyceal system due to intermittent total or continuous partial obstruction to urine outflow across the PUJ.

If there is concomitant dilatation of the ureter, the term hydroureteronephrosis is used.

Causes of Unilateral Hydronephrosis/Hydroureteronephrosis:

1. Intraluminal (within the lumen)

Stones, sloughed papillae (as in diabetics and those with analgesic nephropathy), sloughed urothelial cancer, organized blood clots, chylous balls, fungal bezoars, and inflammatory synechiae may obstruct the lumen to varying degrees.

2. Intramural (in the wall)

1. Congenital
   • PUJ obstruction (PUJ dyskinesia or achalasia of PUJ) is a congenital lesion where hydronephrosis occurs due to failure of transmission of neuromuscular impulses across the PUJ. It may also be bilateral. Male: The female ratio is 2:1. It is more common on the left side. PUJ obstruction may be seen in ectopically placed kidneys as well as in horseshoe kidneys.
   • Ureterocele (cystic dilatation of the terminal ureter), congenital obstructive megaureter (functional obstruction at the level of the vesicoureteric junction, pathology is akin to that which occurs in PUJ obstruction)—both cause hydroureteronephrosis.
2. Acquired
   • Carcinoma of the ureter or carcinoma of the bladder involving the ureteric orifice.
   • Stricture of the ureter secondary to stone: After dislodgement of the stone, there may be inflammatory stricture of the ureter.
   • Tuberculosis of the ureter and bladder.

3. Extramural:

1. Malignant infiltration of the ureter (from cancers of the uterine cervix, rectum, urinary bladder), obstructive encasement as in retroperitoneal tumours, and compression by enlarged lymph nodes (metastatic or primary).

2. Obstruction by aberrant vessels: Aberrant renal artery going to the lower pole of the kidney may cause ureteric obstruction.

3. Retrocaval ureter

4. Idiopathic retroperitoneal fibrosis

Causes of Bilateral Hydronephrosis/Hydroureteronephrosis:

Obstruction below the bladder neck due to any cause may cause bilateral hydroureteronephrosis (intravesical causes). Any cause of unilateral ureteric obstruction when operational on both sides simultaneously may cause bilateral hydronephrosis (supravesical causes). Idiopathic retroperitoneal fibrosis (Ormond’s disease) may cause fibrous encasement of the ureters, which is a rare supravesical cause of bilateral hydroureteronephrosis.

The flow of urine is unidirectional and always towards the bladder from the upper urinary tract. At times, this is reversed, and there is retrograde propulsion of the ureter from the bladder into the ureters.

This is called vesicoureteral reflux (VUR). In severe grades of VUR, there may be bilateral or unilateral hydroureteronephrosis.

Hydronephrosis Common Causes:

1. Causes in Children:

1. Phimosis
2. Meatal stenosis
3. Posterior urethral valve
4. Bilateral vesicoureteric reflux

2. In young adults:

• Stricture urethra was commonly due to gonococcal urethritis. Iatrogenic strictures following instrumentation of the urethra and those which develop following rupture urethra are becoming more common.
• Bilateral aberrant vessels: Quite often, these may be the branches of the renal artery and vein which cross the ureters.

3. Causes in middle age and above:

• Benign prostatic hypertrophy (BPH)
• Bladder neck contracture
• Idiopathic retroperitoneal fibrosis (Ormond’s disease)

4. Physiological: Pregnancy

Compression due to a growing gravid uterus and the relaxant effect of progesterone on ureteric smooth muscle.

Hydronephrosis Pathogenesis

The back pressure effect depends on the type of pelvis.

1. In patients with an intrarenal pelvis, the kidney gets damaged very early. As time goes on, the urine in the collecting system gets diluted. All the salts are absorbed and replaced by a watery type of fluid having a specific gravity of 1.010.

2. Patients with an extrarenal pelvis have minimal damage to the renal parenchyma for a long time.

3. Even with complete obstruction, glomerular filtration occurs to an extent, resulting in the production of some amount of urine. This is opposed by the rising pressures in the pelvis. To maintain filtration and protect the renal parenchyma from harmful pressure effects, several back flow mechanisms are pressed into service. The important decompression mechanisms are pyelosinus, pyelovenous, pyelolymphatic, pyelotubular and pyelointerstitial backflows. Back flows occurs across the epithelial membranes between two anatomical structures through microscopic discontinuities called ‘backflow breaks’.

Further progression of the disease leads to a nonfunctional kidney.

Acute bilateral obstructions present with symptoms of uremia, and untreated bilateral obstructions lead to chronic kidney disease (CKD) over time.

Hydronephrosis Clinical Features:

1. Painless enlargement of the kidney. A renal mass is felt in the loin. It has a smooth surface and is firm in consistency (tensely cystic).
2. Dull-aching pain in the loin.
3. Previous history of calculus disease.
4. Hypertension and haematuria are rarely seen.

5. Dietl’s crisis:

• It is a clinical phenomenon of intermittent hydronephrosis.
• It is common in calculous hydronephrosis.
• Following an attack of renal colic, ureteric obstruction occurs due to a stone, which results in enlargement of the renal pelvis felt as a palpable mass in the loin. After a few hours, the mass disappears due to the passage of a large quantity of urine due to reflux polyuria or due to slippage of the stone.

6. The symptoms of the primary cause may be evident in the history (e.g. colicky radiating abdominal pain due to stones and haematuria).

Hydronephrosis Investigations

1. Plain X-ray KUB

• An enlarged renal outline can be made out
• Demonstration of stone

2. USG can detect enlarged kidneys and the cause of hydronephrosis in most cases.

3. A CT scan is the investigation of choice. It can assess the anatomy and function more accurately than IVU.

4. Intravenous pyelography (IVP):

• Normally, the calyces are concave.
• They become flat and later convex/club-shaped followed by dilatation of the pelvis and ureter depending on the level of obstruction.
• In hydronephrosis with gross impairment of renal function, contrast may not be visible for a few hours on X-ray. In such cases, high doses of contrast (l00– 200 ml) may have to be used, and the pictures may have to be taken even after 24 hours. Such a situation is seen in PUJ dysfunction.

5. Isotope renography: Technetium 99m-labelled DTPA (diethylene triamine penta-acetic acid) scan using a Gamma camerThe above Gamma radiation emitter is injected intravenously. It can be detected in the urinary tract above the level of obstruction and does not get washed off even after giving frusemide injection.

6. Retrograde pyelography (RGP)

• When IVP fails to demonstrate the kidneys, RGP is a useful investigation. It can be done just prior to definitive surgery to confirm the site of obstruction.
• Less quantity of contrast material is required, and better configuration of calyces can be made out.

7. Blood urea and creatinine are estimated to rule out renal failure.

Treatment of Hydronephrosis:

1. Hydronephrosis Secondary to a Cause: Treat the cause.

• Stones: Pyelolithotomy, ureterolithotomy.
• Stricture: Strictureplasty or excision and end-to-end anastomosis.
• Aberrant vessel: Transection of the ureter and anastomosis in front of the vessel.
• Phimosis: Circumcision.
• Meatal stenosis: Meatoplasty.
• Posterior urethral valve (PUV): Transurethral fulguration of the valve.
• Benign prostatic hypertrophy (BPH): Transurethral resection of the prostate (TURP).
• Carcinoma of the prostate: Bladder outlet obstruction (infravesical cause) can be palliated by transurethral channelization. Hydroureteronephrosis can be managed by short-term or long-term DJ stenting along with the institution of options appropriate to the stage (hormonal treatment, radiation therapy, and cytotoxic drugs).
• Stricture urethra: Visual internal urethrotomy or urethroplasty.

Principles of Surgery:

1. Nonfunctioning kidney with thinned out cortex and hydronephrosis/pyonephrosis—nephrectomy.
2. If cortical thickness is adequate (0.5 cm) by ultrasonography, a preliminary nephrostomy should be done to decompress the system. Reassessment of renal function is done after a few days. If renal function improves, definitive surgery for hydronephrosis can be done. If it remains a nonfunctioning kidney and the opposite kidney is normal, nephrectomy is done.
3. In bilateral hydronephrosis, the better functioning kidney should be operated first. An exception to this principle is when the relatively poor functioning kidney is a seat of sepsis, for which some means of drainage by either DJ stenting or percutaneous nephrostomy should be done before definitive correction of the better functioning side.

2. Patients with Congenital Hydronephrosis—Pelviureteric Junction (PUJ) Dysfunction:

Congenital hydronephrosis needs special mention here. With the increasing use of obstetric ultrasound, the incidence of antenatally detected foetal hydronephrosis is on the rise. Antenatal detection of foetal hydronephrosis has become the most common mode of presentation of congenital hydronephrosis.

Congenital hydronephrosis is defined as the anteroposterior diameter of the renal pelvis > 10 mm at > 20 weeks of gestation. PUJ obstruction is the main cause. These foetuses undergo serial ultrasound monitoring during the rest of pregnancy. Based on the increase or decrease in the pelvic diameter during this period, postnatal management can be planned even before the child is born.

Indications for Surgery:

Grades of Renal Pelvic Diameter and Management:

• 1 Mild 11–20 mm
• 2 Moderate 21–35 mm
• 3 Severe > 35 mm
• Grade 1 hydronephrosis can be managed conservatively by serial monitoring of the pelvic diameter by ultrasound and renal function by DTPA scan. These kidneys improve over a period of time.
• Grade 2 hydronephrosis: The majority (almost 80–90%) may be managed conservatively. However, close monitoring of the patient is required to detect any deterioration in renal function, which is an indication for surgical intervention. In this group, 10–20% of patients benefit from early surgery (patients with renal function of the involved kidney < 40%).
• Grade 3 hydronephrosis: All these patients should be operated early—modified Anderson-Hynes pyeloplasty to prevent permanent damage to the kidney.

Types of Pyeloplasty (Modified Anderson-Hynes):

This is the most popular type of dismembered pyeloplasty.

1. Dismembered Pyeloplasty—Anderson-Hynes Pyeloplasty

Principles (Foley Criteria):

1. Excision of the redundant pelvis (pelvic reduction)
2. Excision of the dysfunctional PUJ segment.
3. New ureteropelvic anastomosis is done in such a way that urine drains by gravity.
4. Watertight anastomosis.

2. Nondismembered Pyeloplasty:

• Foley’s Y-V plasty or flap pyeloplasty, in which the PUJ is not transected, are not very popular.

3. Endoscopic Pyeloplasty:

It can be done if the stricture is < 2 cm.

Renal Tuberculosis (TB):

• This is secondary to pulmonary TB/lymphatic TB.
• The primary focus is often difficult to identify.
• Common in males aged 20–40 years.
• Infection is always haematogenous. One may not find any active lesion in the lung or lymph nodes.
• Usually unilateral.

Hydronephrosis Pathology:

1. Tubercles develop and coalesce over the papilla, which may ulcerate—ulcerative form.
2. Tubercles may caseate and rupture over the renal papilla and communicate with the pelvis— ulcerocavernous form.
3. Attempt at healing produces calcification— pseudocalculi in the parenchyma of the kidney.
4. Tubercular hydronephrosis is very rare. It is due to tubercular stricture of the PUJ.
5. The opening of one of the calyces may get fibrosed leading to hydrocalyx, which may distort the rest of the calyces.
6. A cortical abscess ruptures into the perinephric space and forms a tubercular perinephric abscess.
7. This may point at the loin and rupture to form a sinus.
8. Tubercular pyonephrosis (caseous kidney, putty kidney, cement kidney). When it gets calcified, it is called cement kidney. The entire kidney is converted into a bag of pus, which is tubercular caseous material with or without secondary infection. A complete ureteric stricture due to tuberculosis cutting off the pelvicalyceal system may result in autonephrectomy because of fibrosis.
9. Small, fibrosed, contracted, functionless kidney.
10. As a part of miliary tuberculosis—multiple small tubercles may be seen in the renal parenchyma.

Hydronephrosis Clinical Features:

1. Frequency is the earliest symptom of tuberculosis. It is due to renal tubular inflammation (concentrating ability is affected, hence polyuria) and later due to tubercular cystitis.
2. Abacterial acid pyuria: The urine is opalescent, pale or yellow, and acidic in reaction. No organisms/ bacteria are grown on repeated conventional culture.
3. Haematuria is not uncommon. Usually it is of small quantity due to ulcerocavernous variety.
4. Evening rise of temperature.
5. Loss of appetite and loss of weight.
6. Evidence of pulmonary or lymph node TB may be present.

Hydronephrosis Investigations

1. Urine for acid-fast bacilli (AFB):

• A sample of first-voided urine in the morning has to be examined to give the highest yield of AFB for 3 days.
• Ziehl-Neelsen staining and Gram staining (conventional, not in vogue).
• Lowenstein-Jensen media culture.
• Guinea pig inoculation is positive in 90% of cases.

Photographs Of Renal Tuberculosis

2. Cystoscopy:

1. The earliest sign is pallor around the ureteric orifice.
2. Initially, small ulcers are seen around the ureteric orifice. They join together and result in a larger ulcer.
3. Due to extensive periureteric fibrosis, the ureter becomes thickened, shortened, and straight. The ureteric opening is lifted upwards and gapes (i.e., does not contract/ close when the bladder contracts). Such contracted, elevated, permanently opened, lower end of the ureter is called golf hole ureter.
4. As a result of this, with each bladder contraction, there is urine reflux into the kidney, which causes damage.
5. When the disease affects the urinary bladder, there will be extensive fibrosis. Soon, its capacity and compliance are reduceAt this stage, the patient suffers from strangury, which is painful ineffectual straining of urination culminating in voiding a few drops of urine. This is called “thimble bladder” or “systolic bladder”.

3. IVP: The earliest sign is moth-eaten calyx. Thimble bladder and hydronephrosis may be featuress.

4. CECT: It is the investigation of choice.

Photographs Of Renal Tuberculosis Treatment

1. A conservative line of management with antitubercular treatment is successful, provided the kidneys are functioning as in early stages (it should be pointed out that a full course of antitubercular regimen is integral, regardless of surgical treatment).

2. Nephroureterectomy is indicated if the kidney is nonfunctioning.

3. Renal cavernotomy of Henley:

• Indicated when there is stricture of calyces resulting in hydrocalyx.
• In this operation, the stricture is divided so that drainage improves.

4. Treatment of thimble bladder—ileocystoplasty:

• A 10–15-cm ileal loop is isolated based on the blood vessels, the fibrosed bladder dome is excised, and the intestine is split open and sutured to the urinary bladder.
• This increases the capacity of bladder to store urine, thereby reducing frequency.

5. Boari flap for ureteric stricture.

Renal Neoplasms

Renal Neoplasms Classification

• Benign: Adenoma, cortical adenoma, papilloma arising from the pelvis, haemangioma.
• Malignant: Nephroblastoma, renal cell carcinoma
• Transitional cell carcinoma (rare)
• Squamous cell carcinoma (extremely rare)

Wilms’ Tumour (Nephroblastoma)

• This is a malignant tumour of the kidney that occurs in children.
• The tumour is composed of epithelial and mesothelial elements. It comprises blastemal, epithelial, and connective tissue (bone, cartilage, and muscle). Hence, it is called nephroblastoma (immature embryonic tissue).
• The tumour arises in one of the poles and distorts the reniform shape of the kidney. It is greyish-white or pinkish-white in colour (resembles brain tissue). At places, there may be areas of haemorrhage/ necrosis.
• Microscopic features include connective tissue elements, cartilage, spindle cells, smooth striated muscle cells, and epithelial elements.
• 5% are bilateral.
• It occurs in familial and nonfamilial forms.

Wilms’ Tumour Clinical Features

• Both males and females are equally affected around 2–4 years of age.
  • If it occurs at < 1 year of age, it has good prognosis.
  • The upper age limit is 7 years.
  • Rarely, it may occur in adolescents.
• The child presents with abdominal distension due to a huge, nodular kidney.
• Rarely, Wilms’ tumour can be bilateral.
• Haematuria is a poor prognostic symptom. It indicates rupture of the tumour into the renal pelvis.
• Such children usually die by 2 years of age.
• Low-grade fever may occur in rapidly growing tumours due to tumour necrosis, which releases pyrogens.
• Rapid deterioration of health is characteristic.

Wilms’ Tumour Investigations

1. Abdominal USG may detect a solid tumour in the kidney. Ultrasound rules out a tumour in the opposite kidney.
2. CT scan—to know the extent of lesion and spread to the adjoining structures.
3. IVP is done to study distortion of calyces and to evaluate the function of the opposite kidney (CECT urogram has supplanted this).
4. FNAC is done to preoperatively confirm the diagnosis.

Wilms’ Tumour Differential Diagnosis

1. Neuroblastoma arises from adrenals. This is more common than nephroblastoma.
2. Retroperitoneal tumours
3. Adrenal tumour

Differentiating features between Wilms’ tumour and neuroblastoma (NBL):

• Calcification—foci of calcification seen in NBL (85%).
• Less common in Wilms’ (15%).
• Intraspinal extension—seen in NBL
• Aorta and IVC invasion by Wilms’
• Location
  • Wilms’—intrarenal
  • Neuroblastoma—seen above the kidney pushing it downwards and outwards.
• Crossing the midline—neuroblastoma
• Urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) increase in neuroblastoma.

Spread:

1. Direct infiltration of the capsule
2. Lymphatic spread occurs to the hilar, para-aortic, mediastinal, and left supraclavicular lymph nodes.
3. Haematogenous spread occurs to the lungs, liver, bones, brain, etThe tumour thrombus can extend to the renal vein and inferior vena cava.

Wilms’ Tumour Treatment

Anaemia has to be corrected as soon as possible.

1. For tumours confined to the renal capsule or perirenal soft tissue not infiltrating the adjacent organs, radical nephrectomy followed by chemotherapy with actinomycin D and vincristine is given for 6 months.
2. For tumours that extend beyond the renal capsule and perirenal soft tissue, have local infiltration to adjacent tissue, or have lymphatic metastasis, nephrectomy followed by local radiotherapy and chemotherapy are given with actinomycin D and vincristine for 15 months.
3. If the tumour is found to be unresectable by CT or MRI, preoperative FNAC to confirm the diagnosis is indicated, followed by preoperative radiotherapy (1000 cGy) or chemotherapy. Once the tumour regresses in size, a nephrectomy should be done. Postoperative chemotherapy is given with actinomycin D, vincristine, and doxorubicin.
4. Bilateral Wilms’ tumour: Radical nephrectomy on the side of the larger tumour and partial nephrectomy on side of the smaller tumour should be done. As much renal tissue as possible should be preserved after leaving a tumour-free margin. Postoperatively, the patient should be treated with chemotherapy. When surgery is not feasible, only radiotherapy and chemotherapy should be given. Growth disturbances and cardiac and pulmonary toxicities are complications of radiotherapy.

Renal Cell Carcinoma (RCC)

• It is also called hypernephroma or Grawitz tumour.
• Peak incidence at 60–70 years. Extensive use of ultrasound imaging for nonspecific abdominal symptoms has led to earlier pickup of this tumour in the fourth and fifth decades of life.
• Male: female ratio 2:1.
• It occurs in sporadic (common) and hereditary (rare) forms.

Aetiology:

The exact aetiology of sporadic RCC is unknown. Several environmental factors have been incriminated, such as urban dwellings, low socioeconomic status, tobacco chewing, cigarette smoking, exposure to asbestos, and analgesic abuse (phenacetin).

Comorbidities like renal failure/dialysis, obesity, hypertension, and diabetes are known to increase the risk.

In the hereditary or familial forms, specific oncogenes are operational. von Hippel-Lindau syndrome, in which tumorigenesis results due to loss of a tumour suppressor gene, is a well-known example of this form of RCA papillary variant of RCC occurs as a familial form which is characterized by trisomy 7 and 17 and is due to activation of a proto-oncogene.

Wilms’ Tumour Pathology:

• Nearly all RCCs in adults are adenocarcinoma.
• Cell of origin: Proximal convoluted tubular epithelium.
• Starts in one of the poles (commonly in the upper pole) and usually ruptures outside the capsule, because of which the reniform shape of the kidney is maintained (Wilms’ tumour grows within the capsule. Hence, the kidney shape is lost very early).
• On the outer surface, it is homogenous (Wilms’ tumour is pleomorphic) and yellow in colour due to lipid deposition.
• A few haemorrhagic areas are common because the tumour is very vascular.
• Microscopy: Alternate clear cells and dark cells.

Various Subtypes of RCC:

1. Clear cell carcinoma
   • Most common type (70–80%)
   • It may be familial, associated with von HippelLindau syndrome, or sporadic (95%).
2. Papillary—both familial and sporadic forms.
3. Chromophobe—arises from the cortical portion of the collecting duct. These tumours exhibit multiple chromosome losses and extreme hypoploidy.
4. Renal medullary carcinoma:
   • New subtype
   • Associated with sickle-cell trait
   • Arises from calyceal epithelium.
   • Carries a poor prognosis.
5. Collecting duct (Bellini)—rare, occurs in young, has poor prognosis. The term “sarcomatoid” is used to describe an infiltrative and poorly differentiated variant of any of the above types.
6. Tumour cells line the blood vessels which are responsible for early blood spread from renal cell carcinoma (like follicular carcinoma of the thyroid— angioinvasion and capsular invasion).

Wilms’ Tumour Clinical Features:

1. Triad of Renal Cell Carcinoma:

Triad is seen in only 9%, but if present, it strongly indicates metastatic disease.

1. Pain: Dragging or intermittent colic due to blood clot blocking the ureter.
2. Intermittent haematuria
3. Palpable mass: Hard, nodular, ballotable, and bimanually palpable loin mass that moves with respiration.

2. Other Manifestations:

1. Pathological fractures (e.g. fracture femur, humerus)— vascular, pulsatile, secondaries are common in flat bones (e.g., scalp, vertebra, rib, sternum) because they contain red marrow for a longer time.

2. Anaemia is disproportionate to the amount of haematuria due to decreased production of erythropoietin.

3. Mild elevation of temperature due to tumour necrosis, which produces pyrogens. It can present as pyrexia of unknown origin (PUO) and is hence called internist’s tumour.

4. Nephrotic syndrome-like features are rare.

5. Endocrinal disturbances (paraneoplastic syndromes) are rare. Increased ESR—most common paraneoplastic syndrome.

• Renin-producing tumours are responsible for hypertension.
• Polycythaemia is due to increased erythropoietin secretion.
• Other hormones produced by the tumour are parathormone, adrenocorticotrophic hormone, human chorionic gonadotropin, glucagon, and prolactin.

6. Hypertension

7. Liver dysfunction: Nonmetastatic liver dysfunction (increased liver enzymes), also known as Stauffer’s syndrome, improves after nephrectomy (deranged enzymatic levels normalize).

Robson’s Staging of Renal Cell Carcinoma

• Stage 1: Tumour limited to the kidney
• Stage 2: Tumour invading the perinephric tissues or adrenal gland, but not extending beyond the Gerota’s fascia.
• Stage 3: Tumour extending into major veins or involving lymph nodes.
• Stage 4: Tumour invasion beyond Gerota’s fascia or with distant metastasis.

Wilms’ Tumour Investigations

1. Urine examination when the patient has haematuria to look for malignant cells. In RCC, urine cytology is negative. If positive in a patient with haematuria, urothelial cancer should be suspected.
2. Plain X-ray KUB region: Enlarged kidney shadow can be seen (enlarged renal silhouette).
3. IVP: Distortion of calyces, missing calyces, or loss of the architectural pattern of the kidney.
4. USG
   • Enlarged kidney.
   • Locate the tumour, site, and extent.
   • USG-guided FNAC can be done.
   • Can detect thrombus in the inferior vena cava (IVC).
   • In the real-time examination, the IVC collapses during inspiration and opens during expiration. This is called caval kinetics. When the tumour thrombus extends into the IVC, this feature is lost in the segment housing the thrombus.

5. Contrast-enhanced CT scan is the investigation of choice for staging.

6. Renal angiography is done by a retrograde transfemoral approach. Features are as follows:

• Neovascularisation: Tumour blush inside the tumour.
• The venous phase has to be observed to rule out tumour extension in the vein.

7. MRI scan: MRI is the investigation of choice to know the extent of IVC thrombus (better than CT).

8. Venacavogram: It is done to know extent of tumour in the IVC and the presence of collateral circulation.

9. Chest X-ray—rarely done as lung fields are surveyed during CT. Pulmonary metastases on chest X-ray are described as “cannonball lesions.”

Wilms’ Tumour Treatment

1. Radical nephrectomy:

• Enbloc removal of the entire Gerota’s fascia with its contents (i.e. kidney, proximal ureter, adrenal gland).
• Retroperitoneal lymph node dissection does not improve the survival rate.
• Routine removal of the ipsilateral adrenal gland is uncommon unless the tumour involves a large portion of the upper pole of the kidney or preoperative radiologic exams suggest adrenal gland involvement.

2. Radical nephrectomy with extraction of tumour thrombus:

• The tumour thrombus may extend along the renal vein into the IVC and even into the right atrium.
• Infradiaphragmatic tumour thrombus can be removed with proximal control over the vena cava.
• Supradiaphragmatic IVC thrombus requires a cardiopulmonary bypass.
• In the absence of distant metastasis after thrombus removal, these patients survive for a long duration.

3. Nephron-sparing surgery: It is done in tumours <4 cm, in bilateral tumours, in those with comprised renal function, in familial RCCs, and in cases of renal cell carcinoma in solitary kidney.

4. Therapeutic embolisation:

• This can be used as a palliative measure in advanced carcinoma to relieve symptoms. This can also be used preoperatively to regress the size of large tumours.
• A catheter is placed in the renal artery, and substances such as gel foam, blood clot, and crushed muscle are injected.
• They block the lumen of the vessel and reduce the size of the tumour so that radical nephrectomy can be performed later.

5. Radiotherapy: Not of much use. However, it is a good form of palliation for secondaries in the lung, bone, and brain.

6. Immunotherapy: Administration of interferon or interleukin-2 has been found to improve the survival rate. Transitional cell carcinoma of the renal pelvis.

Renal Mass In The Surgical Ward

Clinical Features of Kidney Mass:

• Moves with respiration because the fascia of Gerota encloses the kidney and fuses above the diaphragm.

Renal mass in the surgical ward:

• Kidneys enlarge in the upward and downward direction.
• Bimanually palpable and ballotable. It is ballotable because of the renal pedicle and perirenal pad of fat.
• The colonic band of resonance is obliterated when the kidney enlarges, as the colon is pushed laterally.

The upper border is not palpable because it is under the 12th rib.

Acute Surgical Infections Of The Kidneys

Pyonephrosis

In this suppurative inflammatory condition, the entire kidney is converted into a sac containing pus or purulent urine—the renal parenchyma is almost always completely destroyed.

Acute Surgical Infections Of The Kidneys Causes

1. Renal calculous disease is the most common cause of pyonephrosis.
2. Acute pyelonephritis is more common in children and in females. Inadequately treated cases may develop into pyonephrosis, especially when pyelonephritis is associated with urinary tract obstruction.
3. Infection of hydronephrosis.

Acute Surgical Infections Of The Kidneys Clinical Features:

• Anaemia and fever
• Renal swelling
• Large swelling with high-grade fever with chills and rigors suggests an imminent danger of septicaemia and requires immediate drainage of pus.

Acute Surgical Infections Of The Kidneys Investigations:

• Urine examination may be positive for coliforms and other gram-negative organisms.
• Plain X-ray KUB may reveal a stone or an enlarged renal outline.
• Ultrasound can confirm hydronephrosis.
• Intravenous urogram demonstrates poor function of the kidney on the diseased side. As a rule, the opposite kidney is normal.
• CECT is the investigation of choice.

Acute Surgical Infections Of The Kidneys Treatment:

• Broad-spectrum antibiotics (parenteral) should be started immediately once urine and blood are sent for culture and sensitivity.
• Ultrasound-guided aspiration of pus or a percutaneous nephrostomy (preferred) and drainage of pus greatly improves the general condition of the patient.
• If any obstruction or causative agent such as a stone is found, it should be removed.
• A nephrectomy should be considered if the kidney is non-functioning with significant damage.

Perinephric Abscess

It refers to the collection of pus in the perirenal area.

Acute Surgical Infections Of The Kidneys Causes:

• Infection in a perirenal haematoma
• Pyonephrosis after rupture
• Tubercular perinephric abscess
• Pus from retrocaecal appendicitis may extend into the loin and perinephric area, and may present as an abscess.

Acute Surgical Infections Of The Kidneys Clinical Features:

• High swinging temperature
• Rigidity, tenderness, and fullness in the loin
• Oedema in the loin

Acute Surgical Infections Of The Kidneys Investigations:

• Total count: > 20,000 cells/mm3
• Urine analysis: No organisms are usually found
• X-ray spine: Scoliosis with concavity towards the abscess
• Screening chest: Diaphragm is immobile and elevated on the diseased side.

Acute Surgical Infections Of The Kidneys Treatment:

Broad-spectrum antibiotics are started first. Ultrasound-guided pigtail insertion or percutaneous drain insertion should be attempted if it fails, create an incision in the loin, drain the pus, and break all loculi. Closure is done with a drain. Once pus culture is available, treat accordingly.

Miscellaneous

Kidney And Ureter Multiple Choice Questions

Question 1. Which of the following is not a feature of adult polycystic kidney disease?

1. It may cause renal failure
2. Hypertension is seen in about 75% of patients
3. It is autosomal recessive
4. It is always bilateral

Answer: 3. It is autosomal recessive

Question 2. Relations of the right kidney include the following:

1. Muscles posteriorly
2. Pyloric antrum anteriorly
3. Ascending colon laterally
4. Adrenals medially

Answer: 2. Pyloric antrum anteriorly

Question 3. Which of the following is a feature of horseshoe kidney?

1. Classically, it is the upper polar fusion of both kidneys
2. It does not cause angulation of the ureter and hydronephrosis
3. It may be associated with Down’s syndrome
4. Hyperextension of the spine results in pain, nausea, and vomiting

Answer: 4. It may be associated with Down’s syndrome

Question 4. Gout results in:

1. Calcium stones
2. Cystine calculi
3. Phosphate
4. Uric acid stones

Answer: 4. Uric acid stones

Question 5. Which type of stone typically causes haematuria?

1. Oxalate
2. Phosphate
3. Cystine
4. Uric acid

Answer: 1. Oxalate

Question 6. The following are true for calcium oxalate stones:

1. They are called mulberry calculi
2. They are smooth and round
3. They are hard
4. They are visible on X-ray

Answer: 2. They are smooth and round

Question 7. The following are true about uric acid stones:

1. They are common in those who consume red meat
2. They are small and multiple
3. They are also seen in gout
4. Pure uric acid stones are radio-opaque

Answer: 4. Pure uric acid stones are radio-opaque

Question 8. What type of stone is Staghorn calculi?

1. Calcium oxalate
2. Phosphate
3. Uric acid
4. Cystine

Answer: 2. Phosphate

Question 9. Which of the following is not an ideal treatment for upper ureteric stones?

1. ESWL
2. Percutaneous removal
3. Ureteroscopic removal
4. Cystoscopic removal

Answer: 1. ESWL

Question 10. A patient presents with renal stones and a swelling in the neck. What is the likely diagnosis?

1. Medullary thyroid carcinoma
2. Hyperparathyroidism
3. Hyperthyroidism
4. von Recklinghausen’s disease

Answer: 2. Hyperparathyroidism

Question 11. Which of the following causes bilateral hydronephrosis?

1. Idiopathic retroperitoneal fibrosis
2. Carcinoma ureter
3. Tuberculosis of the urinary tract
4. Aberrant artery

Answer: 1. Idiopathic retroperitoneal fibrosis

Question 12. The following are features of Dietl’s crisis except:

1. It is called intermittent hydronephrosis
2. It is usually seen in calculus hydronephrosis
3. It does not produce a mass
4. It occurs due to stone slippage

Answer: 3. It does not produce a mass

Question 13. Which is the investigation of choice in hydronephrosis?

1. Ultrasound
2. Intravenous pyelography
3. CT scan
4. Isotope renography

Answer: 3. CT scan

Question 14. Definite indications for pyeloplasty include the following:

1. Calculus hydronephrosis
2. Grade 3 hydronephrosis
3. Nonfunctioning kidney with a cortical thickness of 0.1 cm
4. Tuberculous hydronephrosis

Answer: 2. Grade 3 hydronephrosis

Question 15. The following are true for renal tuberculosis except:

1. It is a primary tuberculosis
2. Infection occurs by lymphatic spread
3. It commonly causes hydronephrosis
4. It causes bacterial acid pyuria

Answer: 4. It causes bacterial acid pyuria

Question 16. Which of the following is an uncommon symptom of renal tuberculosis?

1. Haematuria
2. Evening rise in temperature
3. Cystitis
4. Pyuria

Answer: 1. Haematuria

Question 17. The following are complications of renal tuberculosis:

1. Thimble bladder
2. Golf hole ureter
3. Putty kidney
4. Hydronephrosis

Answer: 4. Hydronephrosis

Question 18. The following are true for Wilms’ tumour:

1. It contains only epithelial elements
2. It commonly presents before 1 year of age
3. Its prognosis is poor if it occurs within 1 year of age
4. Haematuria indicates poor prognosis

Answer: 4. Haematuria indicates poor prognosis

Question 19. The following are true about renal cell carcinoma except:

1. It is mainly adenocarcinoma in adults
2. Reniform shape of the kidney is maintained
3. Clear cells and dark cells are present on microscopy
4. Tumour cells do not line the blood vessels

Answer: 4. Tumour cells do not line the blood vessels

Question 20. Polycythaemia in renal cell carcinoma is due to the production of:

1. Renin
2. Erythropoietin
3. Prolactin
4. Glucagon

Answer: 2. Erythropoietin

Question 21. The diagnostic CT finding of renal cell carcinoma in elderly patients is:

1. Dense mass
2. Tumour necrosis
3. Lymph node enlargement
4. Enhancing mass after intravenous contrast

Answer: 4. Enhancing mass after intravenous contrast

Question 22. The following is true for transitional cell carcinoma except:

1. It is a low-grade tumour
2. Haematogenous spread is common
3. It arises from the urothelium
4. Multiple sites are usually not involved

Answer: 4. Multiple sites are usually not involved