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Home , Obstructive uropathy

The obstructed kidney

Rishi Nayyar, Anil K. Sarda, R. C. M. Kaza, V. J. Anand Department of Surgery, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi - 110002, India

For correspondence: Dr. A. K. Sarda, 27 RPS, Triveni-1, New Delhi - 110017, India. E-mail: [email protected]

ABSTRACT Urinary obstruction is a common cause of acute and chronic renal failure. The symptoms and signs of an obstructed kidney may vary from asymptomatic to severe acute pain. The diagnosis and management of a hydronephrotic kidney is not very difficult with ultrasonography, IVU, and diuretic renography. The approach to manage such patients has been rationalized after the advent of diuretic renography. The obstructed kidney should be decompressed as early as possible because of progressive loss of renal function with prolonged obstruction. Nephrectomy may be required for a non-functioning kidney. Further advancements are being made as the molecular mechanisms involved in the pathophysiology of the obstructed kidney become known to us.

Key Words: Obstructive uropathy, hydronephrosis, intravenous urography, diuretic renography, non-visualized kidney,

Review Article non-functioning kidney, nephrectomy, ureteral stent, nephrostomy, postobstructive diuresis

Hot to cite this article: Nayyar R, Sarda AK, Kaza RCM, Anand VJ. The obstructed kidney. Indian J Surg 2005;67:21-8.

INTRODUCTION populations. In large surveys of elderly men a prevalence of 20-35% has been estimated for ‘Obstructive uropathy’ refers to the structural symptoms of urinary obstruction. Post-mortem impedance to the flow of anywhere along examinations have found hydronephrosis in 3.8% of the urinary tract leading to ‘hydronephrosis’, adults and 2.0% of children. Obstructive uropathy which is the dilation of the renal pelvis and associated with congenital anomalies of the urinary calyces.[1] Dilatation of the renal pelvis can tract accounts for 30-50% of all end stage renal disease occur even in the absence of urinary cases in children.[4] In women, obstruction is more likely obstruction; therefore, hydronephrosis and to occur at a younger age as a result of pregnancy or obstructive uropathy are not interchangeable uterine cancer. or synonymous terms. The damage to renal parenchyma caused by these conditions often Hydronephrosis is often discovered incidentally on an leads to ‘obstructive nephropathy’ contributing ultrasound conducted for another suspected abdominal to a decrease in renal function.[2] Unlike many disease. No definite data is available on this clinical other renal diseases, obstructive nephropathy, entity and its clinical importance is uncertain, especially if treated early, is a potentially curable form of in Grade 1 or 2 hydronephrosis and in the absence of kidney disease.[3] signs or symptoms of any disease.

INCIDENCE AND EPIDEMIOLOGY AETIOLOGY AND CLASSIFICATION

No data are available on the incidence and There are a multitude of causes of hydronephrosis and prevalence of urinary obstruction in unselected hydroureter (Table 1). Urinary tract obstruction can be classified according to cause (congenital versus acquired), duration (acute versus chronic), degree Paper Received: September 2004. Paper Accepted: October (partial versus complete), and level (upper versus lower 2004. Source of Support: Nil. urinary tract).

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Table 1: Causes of hydronephrosis and hydroureter pressure and dilates the affected regions of the renal Renal pelvis, calyces, and . Increased ureteral pressure Intrinsic also results in pyelotubular, pyelovenous and Intrarenal obstruction Crystals (uric acid, sulfonamide, acyclovir) pyelolymphatic backflow increasing the risk of systemic Protein casts (multiple myeloma, amyloidosis) sepsis in the presence of infection. Hence, obstruction Sloughed papillae coexisting with infection should be considered a Renal cyst and polycystic kidney Renal tumours urological emergency. The dilated kidney is also more Extrinsic predisposed to trauma. Peripelvic cyst Renal artery aneurysm The clinical profile of the patient varies according to Intrinsic 1. the time interval over which the obstruction occurs UPJ obstruction (i.e. acute or chronic), Papillary necrosis 2. whether the obstruction is unilateral or bilateral, Ureteral stricture (iatrogenic) Blood clot 3. the cause of obstruction (i.e. intrinsic vs. extrinsic), Ureteral tumour 4. whether the obstruction is complete or partial, Fungus ball 5. presence of intrarenal versus extrarenal collecting Ureteral calculus system, and Endometriosis 6. presence or absence of infection. Tuberculosis Functional Gram-negative infection Acute urinary obstruction may produce little visible Neurogenic bladder change in the collecting system or renal parenchyma. Extrinsic Chronic obstruction can produce an enlarged, normal Retroperitoneal tumours Cervical cancer or small atrophic kidney, again depending on the Prostate cancer length and degree of obstruction, as well as the presence of an intrarenal or extrarenal collecting Aortic aneurysm system. The intrarenal system, although obstructed to Inflammatory bowel disease Ovarian vein syndrome the same degree and duration as the extrarenal system, Retrocaval ureter may not exhibit the same degree of hydronephrosis; Uterine prolapse however, the degree of renal damage may be worse. Pregnancy Iatrogenic ureteral ligation Usually, the collecting system dilates with time and Ovarian cysts the tissue between the calyces gets thinned out. Diverticulitis Ultimately, the calyces coalesce with thin septa Tuboovarian abscess Retroperitoneal haemorrhage between them and a ‘rim’ or ‘shell’ of parenchyma Lymphocele remains peripherally. Microscopic changes consist of Bladder dilatation of the tubular lumen, flattening of the tubular Intrinsic Bladder carcinoma epithelium and increased collagen deposition in the Bladder calculi peritubular interstitium. Bladder neck contracture Cystocele Primary bladder neck hypertrophy Obstructive nephropathy can lead to kidney failure Functional within a few weeks or a few years. Obstruction Neurogenic bladder maintained for > 6 weeks results in hydronephrosis of the affected kidney with significant irreversible loss of Extrinsic [5] Pelvic lipomatosis functional renal parenchyma. Renal function is also affected by relatively short-term obstructions.[6] Intrinsic Mustonen et al found that glomerular and tubular Extrinsic function partially improved during the first month Benign prostatic hyperplasia following immediate correction of an obstruction.[6] However, months later, half the patients still showed PATHOPHYSIOLOGY glomerular damage, presenting as albuminuria, and tubular damage, presenting as elevated microglobulin Obstructive uropathy occurs when the flow of urine is alpha 1. Animal models have shown that the fibrotic blocked at some point in the urinary tract, and urine and tubular apoptotic processes continue for a few accumulates above the obstruction. This increases the weeks despite the reversal of obstruction.[7]

Indian J Surgery | February 2005 | Volume 67 | Issue 1 22 The obstructed kidney

CELLULAR INFILTRATES AND CYTOKINES IN activation in processes like obstructive uropathy.[4] URETERAL OBSTRUCTION Angiotensin II exacerbates obstructive nephropathy by increasing TGF-β, which promotes both fibrosis and Occupying nearly 80% of total renal volume, the NO degradation.[17,23] tubulointerstitium, the area external to the glomeruli, tubules, and collecting ducts, appears to be the primary EFFECTS OF OBSTRUCTIVE UROPATHY ON area where most damage caused by obstruction GFR occurs.[8,9] This is due to numerous vasoactive inflammatory mediators and growth factors which are Three components determine the GFR: glomerular released as the obstructive nephropathy causes hydrostatic pressure, glomerular colloid osmotic mechanical damage to renal tissue. These include pressure, and Bowman’s capsule pressure. All of these eicosanoids (e.g., prostaglandins, thromboxane A2), can be influenced by an obstruction. During the first angiotensin II, atrial natriuretic peptide, nitric oxide few hours following obstruction, renal blood flow in (NO), endothelin, platelet activating factor, nuclear the obstructed kidney increases secondary to factor kappa B (NF~ kB), and transforming growth preglomerular vasodilatation of renal blood vessels, factor-beta (TGF-β).[8,9,10,11] Cellular infiltrates typically which increases GFR.[1] As the GFR increases, increased involved in obstructive nephropathy include urine formation begins to gradually increase ureteral macrophages, T-lymphocytes, and fibroblasts.[8,12,13] pressure. About 4 hours into the obstruction, renal With chronic obstruction, interstitial fibrosis develops, blood flow declines while ureteral pressure continues creating the most devastating and permanent effects to increase associated with post-glomerular on renal function.[14,15] The prolonged imbalance vasoconstriction.[1] Then, increased intrarenal pressure between the mediators causes excess formation of activates the renin-angiotensin system and increases protein in the interstitial matrix, while there is a levels of vasoconstrictors such as thromboxane A2, deficiency in the mediators required for the destruction which results in decreased renal blood flow and a of protein. The net effect is overproduction of interstitial decrease in ureteral pressure associated with pre- matrix, causing tubular atrophy and decreased numbers glomerular vasoconstriction.[2,8,17] Bilateral ureteric of functioning peritubular capillaries secondary to space obstruction (BUO) differs from unilateral ureteric displacement.[2,15] Decline in both GFR and renal blood obstruction (UUO). While during UUO, the kidney flow following obstruction is also caused by increased passes through these three phases, in BUO the kidney [12,16] levels of thromboxane A2. Tubular cell damage passes through a phase of pre-glomerular occurs as a result of ischemia caused by reduced renal vasodilatation and then a post-glomerular blood flow.[5] Damaged tubular cells further release vasoconstriction and remains in this state. Therefore, substances which attract macrophages and also act on BUO is associated with progressive and persistent rise intact tubular cells to increase the production of in ureteral pressure despite a decrease in renal blood additional inflammatory agents.[17] Although numerous flow. biochemicals are involved in the process, one specific substance, TGF-β, is important.[8,18,19] It is released by Postobstructive diuresis macrophages and attracts fibroblasts, contributing to This phenomenon refers to the marked that the development and proliferation of interstitial occurs after the relief of BUO or obstruction of a solitary fibrosis.[9,20] Recent evidence suggests TGF-β is the kidney. It is most often seen in patients who have primary force driving the increased immunological chronic obstruction, volume overload and sometimes response and the up-regulation of the renin- uremic encephalopathy. Most patients exhibit both angiotensin system during the fibrotic process.[20,21] solute diuresis (caused by retained urea, sodium and TGF-β stimulates the production of NF~ kB, a factor water) as well as a concentrating defect. The associated with tissue inflammation, increased mechanisms responsible for this inability to concentrate angiotensin II production, and the release of tubule urine include high atrial natriuretic peptide levels and cell chemoattractants.[22] It also promotes degradation impaired renal response to vasopressin. of NO. Normally, NO protects the kidney from infiltration of macrophages into the interstitium and CLINICAL FEATURES decreases the production of the protein interstitial matrix, suggesting it may have antifibrotic effects in The signs and symptoms of urinary obstruction depend the kidney.[4] Also, NO inhibits excessive on the parameters already discussed. The vasoconstriction initiated by renin-angiotensin differentiation between acute or chronic obstruction is

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purely clinical. Chronic obstruction is usually all microglobulin alpha-1 filtered by the glomerulus is asymptomatic. When the obstruction is bilateral, reabsorbed by the proximal tubule.[6] With renal patients may present with uremia. Most acute calculus or tumour involvement, microscopic hematuria obstructive uropathies, on the other hand, are is possible, but gross hematuria is unlikely.[29] Chronic associated with significant pain or the abrupt diminution obstruction leads to renal tubule damage, and the of urine flow. The severity of the pain depends on the urinary chemistry findings are similar to those in intrinsic rate of distention more than the amount of dilation of renal failure. These findings include urinary sodium the renal capsule.[24] Patients describe a colic pain in greater than 20 mEq/L, fractional excretion of sodium the flank that increases with consumption of large (FE Na) greater than 1%, urine to plasma creatinine amounts of fluid or following diuretic administration. ratio of less than 20 and urine osmolality less than 350 [1] frequently occurs in acute obstruction and less mOsm/kg H2O. With acute obstruction the urinary frequently in chronic situations.[25] Sometimes, in chemistry values are similar to those in prerenal unilateral obstruction or partial bilateral obstruction, the azotemia. These findings include urinary sodium less patient may notice significant increases in urinary than 20 mEq/L, FE Na less than 1%, urine to plasma output independent of fluid intake related to the creatinine ratio of greater than 30 and urine osmolality [1] [25] damaged kidney’s inability to concentrate urine. greater than 500 mOsm/kg H2O. Microscopic evaluation of the urine may reveal erythrocytes, The clinician needs to obtain a detailed history about leukocytes, and bacteria. the type and duration of symptoms, hematuria, lower urinary tract symptoms, previous urinary tract infections Blood tests include complete blood counts, hematocrit, + - + - (UTIs), history of stone disease, family history of haemoglobin, serum electrolytes (Na , Cl , K , HCO3 , ++ - ++ prostate or pelvic cancer, and urinary output patterns. Ca , HPO4 , Mg ), creatinine, blood urea nitrogen The presence of infection should always be considered (BUN), uric acid, albumin and ABG.[1] The WBC count as it may require emergent drainage. assesses for possible inflammation or infection secondary to obstruction or neoplasm as a cause of Examination may reveal volume overload.[24] There may the obstruction. The hematocrit is important to assess be a palpable abdominal mass with or without for anaemia related to chronic renal insufficiency.[29] costovertebral tenderness, related to hydronephrosis. Patients with increasing serum creatinine without Hydronephrosis that causes the kidney to expand significant proteinuria, and trace to moderate numbers enough to become palpable usually is related to a of red blood cells in the urine should immediately be chronic condition.[25] The bladder may be palpable suspected of having an obstruction.[24] secondary to obstruction low in the urinary tract. Women presenting with suspected urinary obstruction RADIOLOGICAL EVALUATION should always receive a complete pelvic examination, and both genders receive a rectal examination.[1] In Ultrasonography has become one of the most pregnant females, symptoms of frequency, dysuria, important tools for assessing urinary tract obstruction nausea, vomiting or back pain may be present even in because it is rapid, low-cost, safe and sensitive. It is a normal pregnancy. So, urological management is the diagnostic modality of choice in pregnancy.[27] The required only in pregnancy hydronephrosis test is 98% sensitive for detecting hydronephrosis, but complicated by strong flank pains or urolithiasis or the specificity is 78%.[30] Though operator-dependent, pyelonephritis.[26,27] ultrasound detects the type and level of the lesion, shows hydronephrosis, can indicate pyonephrosis LABORATORY EVALUATION (echoes within the collecting system) and tells the thickness of the renal parenchyma as an indicator of Urinalysis results may be normal in both acute and the duration and severity of obstruction. Since up to chronic obstructions. Albuminuria may be absent but 22% cases of hydronephrosis are not obstructive, there is commonly present in the range of less than 1.5 g/ is room for error.[30] Dilation without obstruction may 24 hours reflecting the increased glomerular be seen in vesicoureteral reflux, chronic massive permeability during urinary retention.[6] Even sparse diuresis, extrarenal pelvis, calyceal diverticula, albuminuria indicates glomerular dysfunction.[28] congenital megacalyces and ileal conduits. Obstruction Microglobulin alpha-1, a low molecular weight protein, without dilation may be seen in intrarenal crystals, is an indicator of tubular dysfunction. Normally, nearly nephrocalcinosis, staghorn calculi and retroperitoneal

Indian J Surgery | February 2005 | Volume 67 | Issue 1 24 The obstructed kidney obstruction. Non-contrast computerized tomography (CT) scan is an effective imaging tool for acute renal obstruction. Use of duplex Doppler ultrasonography allows With spiral scanners, images can be performed determination of the renal resistive index (RI), [peak effectively without contrast media, take only 5 to 10 systolic velocity – lowest diastolic velocity] / peak minutes to perform, and cost about the same as IVPs. systolic velocity. An RI in the obstructed kidney that is In terms of benefits, the CT equals the accuracy of the 0.1 greater than the contralateral kidney is considered IVP in determining the presence of obstruction, but significant enough to indicate obstruction. The RI along surpasses the IVP in detecting the specific cause of the with the colour Doppler to show the ureteral jet obstruction.[34] Various signs of obstruction on spiral phenomenon, has improved the efficacy of CT include hydroureter, perinephric stranding, ultrasonography in the diagnosis of renal obstruction hydronephrosis, periureteral oedema and renal in patients presenting with acute and for swelling. However, a non-contrast CT does not indicate whom an IVU is not desirable e.g. pregnancy, history function of the kidneys. of contrast-induced allergy or renal failure.[31,32] MRI gives no added advantage over CT scan. In A supine radiograph [KUB] of the abdomen can reveal addition it does not visualise the stone. However, it radio-opaque urinary tract calculi as the cause of correctly identifies the point of obstruction and the non- obstructive uropathy.[33] However, alone it does not calculous causes of obstruction. MR excretory prove the calculi to be the cause of obstruction, it urography is a promising technique which affords misses out radiolucent calculi and radio-opacity due equivalent functional and additional anatomical to any other cause can be mistaken for the urinary information to isotope renography. It is more accurate calculi. than Doppler ultrasound in the assessment of ureteric obstruction in pregnancy and is not associated with Intravenous urogram (IVU) has been the gold standard any risk of exposure to radiation, unlike IVU or renal for the detection of ureteral obstruction. The significant scan.[31,35] difference in IVU compared with ultrasonography is that the IVU shows both increased anatomic detail and Renal scan and diuretic renography is the most reliable functional attributes of the .[1] It tells technique to quantitatively assess the split and total about the exact site of obstruction, its cause, the degree renal function in the presence of hydronephrosis. It is of hydronephrosis, the status of renal parenchyma, a non-invasive study, can be done even in patients guides the best treatment option, and also helps in with deranged renal function, has no risk of contrast- deciding the best surgical approach for a particular induced nephrotoxicity and also has much less patient. However, in view of nephrotoxicity of the radiation exposure than IVP or CT scan. It can also be contrast material, the usefulness of the test for patients used to measure differential function and, therefore, already suspected of having obstructive nephropathy is useful for treatment planning. Moreover, a functional is questionable.[30] Also, poor renal function may render obstruction can be differentiated from an anatomic the test useless because of non-excretion of contrast. cause. It can be used to follow up a patient after relief In general, a serum creatinine level of less than 2 mg% of obstruction. Also, the assessment of renal blood flow is needed. Another dilemma with IVU is the significant provides a sense of whether function may return upon time requirement, up to several hours, for performing relief of the obstruction. However, images from these serial delayed films. Still, IVU remains the most widely scans lack the resolution to define the site of used imaging modality to guide the management of obstruction. patients of obstructed kidney, because of its low cost and easy availability. A kidney which is non-visualized The current radiopharmaceutical agent most widely on IVU (absence of both nephrogram and used is technetium-99m diethylenetriamine even on delayed films taken after 24-72 hours) should pentaacetic acid (99 mTc-DTPA). It is excreted by be assessed with a renal scan before labelling it as a glomerular filtration and is not secreted or reabsorbed non-functioning kidney (single kidney GFR which is not by the renal tubules. Another much more expensive sufficient to take care of body wastes). A kidney may agent is 99 mTc-mercaptoacetyl-triglyine (MAG3), be non-visualized on IVU because of renal agenesis, which offers better anatomical resolution, is more post-nephrectomy, poor function with or without efficiently excreted by the kidney (glomerular + tubular obstruction, or even in the presence of normal function secretion), can be used in case of decreased renal during renal colic leading to renal artery spasm. function, and delivers a lower dose of radiation. Thus

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it is the agent of choice. or DJ stenting.

This study involves injecting a radioisotope and Other investigative procedures may be required monitoring its passage through the upper urinary tract. depending on the cause of obstruction, for example The early uptake of the kidney can be measured and , evaluation for prostatic disease, and indicates unilateral function. The clearance of the micturating cystourethrography for urethral stricture radiopharmaceutical agent from the renal pelvis with or a suspected vesico-urethral reflux. Urine culture and

a T1/2 of <15 min is considered normal, between 15 to sensitivity should always be obtained in infected cases.

20 min is equivocal and T1/2 >20 min indicates obstruction. Lasix (1 mg/kg) is then administered after MANAGEMENT approximately 20 minutes into the study if washout appears delayed. It is called as F+20 technique of Any urinary obstruction should be relieved if the patient diuretic renography. Progressive accumulation despite is symptomatic, associated with infection, high-grade furosemide administration confirms obstruction. obstruction or a bilateral obstruction associated with However, rapid emptying despite an initial delayed elevated BUN and creatinine or uremia. Such patients excretion indicates dilatation without obstruction should be treated on priority basis without undue delay (functional obstruction). A partial excretory response because of progressively increasing renal loss with may indicate either partial obstruction or renal increasing duration of obstruction, as discussed above. dysfunction with an inability to respond to diuretic. The cases associated with infection should be dealt with These can be differentiated by the F–15 technique of urgently. Minimal intervention in the form of diuretic renography i.e. by administering the diuretic percutaneous nephrostomy or DJ stenting is the safest 15 min before the radiopharmaceutical agent. The yet lifesaving procedure in such patients. equivocal response to diuretic due to poor response to diuretic in the F+20 technique, gets converted to Decompression of the urinary tract washout response in this F–15 technique. A recent Decompression of the urinary tract is required when study has shown no differences in the renogram the definitive management of the disease which has patterns of F+0 (giving diuretic and caused the obstruction, is postponed for some period. radiopharmaceutical together) and F-15 It is also indicated in pregnancy, when the conservative investigations.[36] Because the F+0 study is more treatment with analgesics and antibiotics fails, non- practical and shorter, F+0 method is suggested when resolving infection, deteriorating renal function or equivocal results are obtained by an F+20 study or as absence of Doppler evidence of ureteral flow or an a single test when there is only one opportunity to increased RI.[26] It may also be indicated when one is confirm or exclude the presence of obstruction. not sure of the functional status of the obstructed kidney. When urine collected from a decompressed The Whitaker test was considered gold standard for system is greater than 400 ml and shows normal the evaluation of upper urinary tract dilatation, creatinine clearance, subsequent definitive surgery is classically used for UPJ obstruction. But with the advent indicated to correct the obstruction. Intrarenal of diuretic renogram it is not often utilized clinically. It obstruction secondary to crystals or protein casts is is an invasive test requiring a percutaneously placed not amenable to surgical drainage. Maintenance of cannula inside the renal pelvis and a bladder adequate hydration to promote high rates of urine connected to a pressure transducer each. Fluid (saline output to dilute crystals and casts is the main treatment. + contrast) is pushed into the renal cannula at the rate of 10 ml/min. Fluoroscopic monitoring of the anatomic Decompression of the upper urinary tracts (kidney, site of obstruction can also be done. The rise of pressure ureter) is accomplished by cystoscopic placement of a ureteral stent (distal ureteral obstruction) or in the renal pelvis to less than 15 cm H2O is non- percutaneous nephrostomy (proximal or midureteral obstructed, 15 to 22 cm H2O is equivocal and greater obstruction). than 22 cm H2O is diagnostic of obstruction.

Retrograde pyelogram does not interfere with renal Decompression of the lower urinary tract is function. However, this procedure requires anaesthesia accomplished by urethral catheterisation or suprapubic and is associated with the risk of introducing infection catheterisation (open or percutaneous). in an obstructed system. It now has only an adjunctive role in the operating room during ureterorenoscopy Other measures to be performed when the patient is

Indian J Surgery | February 2005 | Volume 67 | Issue 1 26 The obstructed kidney first seen include The definitive management with the decision to 1. Investigate and begin treatment of the life- preserve the kidney, depends upon the particular cause threatening complications of obstructive uropathy of obstruction and may include watchful waiting, (e.g., pulmonary oedema, hypervolemia, urosepsis, endourologic approach, percutaneous minimally hyperkalemia). invasive technique, laparoscopic or conventional open 2. Consult nephrologist to provide emergent surgery. Today the emphasis is on saving as much of hemodialysis, if necessary the functioning renal tissue as is possible. When both 3. Relief of pain with narcotics or NSAIDs; however, kidneys require surgical correction, one cannot allow the possible nephrotoxicity of NSAIDs should be the time-honoured dictates to be followed. Although kept in mind. it is sound advice to operate on the symptomatic or 4. There are many newer experimental approaches the better functioning kidney first, the opposite kidney that are being tried to ameliorate or modify the cannot be allowed to deteriorate further. It is imperative interstitial damage after urinary obstruction. The that the function of the other kidney be sustained by various chemomediators involved in these insertion of a DJ stent or a PCN catheter just prior to processes, e.g. Ang II, TGF-β, or NO are being the time when a definite operative intervention is targeted to reduce and retard the renal damage planned for the symptomatic/better functioning kidney. associated with obstruction. AT I or AT II receptor More experienced surgeons have also repaired both blockers, ACE inhibitors, 1D11 (a monoclonal sides at the same sitting in the past. But its routine antibody to TGF-β), arginine (a precursor of NO) application is questionable. are all being tried but need further studies before their routine clinical use. REFERENCES

1. Walsh PC, Retnik AB, Vaughan ED, Wein AJ. Pathophysiology DEFINITIVE MANAGEMENT of urinary tract obstruction. In: Campbell’s . 7th Ed. Philadelphia: W.B. Saunders Company; 1998. p. 343-60. The first crucial decision to be made is whether to 2. Klahr S. Obstructive nephropathy. Kidney Int 1988;54:286 – 300. remove the kidney or relieve the obstruction. Diuretic 3. Chevalier RL, Klahr S. Therapeutic approaches in obstructive renography, ultrasonography (cortical thickness) and uropathy. Semin Nephrol 1988;18:652-8. possibly even CT may help the clinician in deciding 4. Huang A, Palmer LS, Hom D, Valderrama E, Trachtman H. The this, but the experience of the surgeon in assessing a role of nitric oxide in obstructive nephropathy. J Urol 2000;163:1276-81. clinical situation and per-op findings is the first. At 5. Klahr S. Pathophysiology of obstructive nephropathy. Kidney times, laboratory data may seem to favour salvage, Int 1983;23:414-26. whereas the experience of the urologist favours 6. Mustonen S, Ala-Houhala I, Tammela TLJ. Proteinuria and renal function during and after acute urinary retention. J Urol nephrectomy. On the other hand, there have been 1999;161:1781-4. cases of return of renal function when the kidney was 7. Vaughan ED Jr, Gillenwater JY. Recovery following complete salvaged if cortical thickness was adequate, even chronic unilateral ureteral obstruction: Functional, radiographic and pathological alterations. J Urol 1971b;106:27-35. though pre-operative renography depicted poor renal 8. Klahr S, Morrissey J. The role of growth factors, cytokines, function.[37] and vasoactive compounds in obstructive nephropathy. Semin Nephrol 1998;18:622-32. 9. Klahr S, Purkerson ML. The pathophysiology of obstructive Nephrectomy should be considered if there is nephropathy: The role of vasoactive compounds in the permanent severe loss of ipsilateral renal function (less hemodynamic and structural abnormalities of the obstructed than 10% of total renal function) or there is kidney. Am J Kidney Dis 1994;23:219-23. 10. Border WA, Noble NA. Cytokines in renal disease: The role of development of unmanageable complication in transforming growth factor-b. Am J Kidney Dis 1993;22:105- hydronephrotic kidney, e.g. severe recalcitrant 13. infection (i.e.. pyonephrosis), or trauma to 11. Ong ACM, Fine LG. Tubular-derived growth factors and hydronephrotic kidney. The issue of renal salvage is cytokines in the pathogenesis of tubulointerstitial fibrosis: Implications for human renal disease progression. Am J Kidney more pressing if the patient has bilateral renal Dis 1994;23:205-9. obstruction. Many a times a non-functioning kidney 12. Diamond JR. Macrophages and progressive renal disease in due to a benign cause is detected incidentally. Such a experimental hydronephrosis. Am J Kidney Dis 1995;26:133-40. 13. Ricardo S, Diamond JR. The role of macrophages and reactive kidney warrants nephrectomy if it is associated with oxygen species in experimental hydronephrosis. Semin any of the following– intractable pain, stone disease, Nephrol 1998;18:612-21. haematuria, recurrent infection, uncontrolled 14. Coroneos E, Assouad M, Krishnan B, Troung LD. Urinary obstruction causes irreversible renal failure by inducing chronic hypertension, malignancy, tuberculosis or large tubulointerstitial nephritis. Clin Nephrol 1997;48:125-8. hydronephrotic kidney liable to trauma. 15. Diamond JR, Richardo SD, Klahr S. Mechanisms of interstitial

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