Cases reported "Kidney Failure, Chronic"

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11/19. Radiolucent urinary calculus in a transplant patient: an unsuspected cause of ureteropelvic obstruction.

    The occurrence of nephrolithiasis and nephrocalcinosis in the patient who has undergone a renal transplant is rare and is usually related to parathyroid hypersecretion. A case is presented in which the patient had a radiolucent stone that arose as a result of the use of nonabsorbable sutures. It is clear that nonabsorbable sutures. It is clear that nonabsorbable sutures should be avoided in renal allotransplant recipients.
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12/19. Bilateral metachronous xanthogranulomatous pyelonephritis in end-stage renal failure.

    We report a case of bilateral metachronous xanthogranulomatous pyelonephritis (XGP) in a hemodialyzed patient with end-stage renal failure due to bilateral nephrolithiasis. The XGP was initially diagnosed by computed tomographic (CT) scan, and right nephrectomy was performed. The patient remained clinically stable for the next year. Involvement of the contralateral kidney was again confirmed by CT examination. Both kidneys showed histologic changes compatible with XGP. A coexisting nephrogenic adenoma of the bladder has been attributed to chronic urinary tract infection.
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13/19. Bone biopsy to diagnose hyperoxaluria in patients with renal failure.

    Primary hyperoxaluria is a rare congenital disorder characterized by large quantities of urinary oxalate with resultant nephrocalcinosis and nephrolithiasis and by deposits of calcium oxalate in other organs. Renal failure occurs early in life. Reports of unsuccessful renal transplantation attempts in this disorder underscore the need for antemortem diagnosis. Percutaneous bone biopsy is a relatively new procedure that is easily done at bedside, safe, and of potentially high yield in the demonstration of tissue oxalate. Three cases presented here show the characteristic histologic picture seen in this disease. In one case, the diagnosis was established by bone biopsy.
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14/19. Bone changes in end-stage oxalosis.

    Primary hyperoxaluria is a rare metabolic disease characterized by exaggerated production of oxalic acid. Clinically the disease is characterized by recurrent calcium nephrolithiasis, progressive renal failure, and early death in uremia. As the regular dialysis treatment may prolong survival, a new syndrome may develop. This is due to intense and continuous deposition of calcium oxalate crystals in soft and bone tissues. The radiologic aspects of oxalate deposition in four adult patients on chronic renal dialysis with histologic and clinical evidence of massive bone oxalosis are reported.
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15/19. hypercalcemia and nephrolithiasis provoked by serum phosphorus reduction in a patient with chronic renal failure and sarcoidosis.

    A patient with sarcoidosis and chronic renal failure was treated for hyperphosphatemia with aluminum hydroxide. The subsequent fall in serum phosphorus was followed by the development of hypercalcemia and nephrolithiasis. Corticosteroid therapy normalized the serum calcium and halted the progression of the nephrolithiasis, but did not improve renal function. hyperphosphatemia may have blocked the expression of sarcoid hypercalcemia in the patient. The mechanism is unclear but inhibition of the synthesis or action of 1,25-dihydroxyvitamin D may have been involved. Reduction of serum phosphorus may lead to severe hypercalcemia in some patients with sarcoidosis.
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keywords = nephrolithiasis
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16/19. adenine phosphoribosyltransferase deficiency with renal deposition of 2,8-dihydroxyadenine leading to nephrolithiasis and chronic renal failure.

    Homozygous adenine phosphoribosyltransferase deficiency is a genetic defect that is associated with 2,8-dihydroxyadenine urolithiasis. Since the prevalence of the heterozygous state is found in 0.4% to 1.2% of the population, it is surprising that more cases of 2,8-dihydroxyadenine urolithiasis have not been reported. Herein we describe a patient with complete adenine phosphoribosyltransferase deficiency with 2,8-dihydroxyadenine urolithiasis leading to chronic renal failure. Gene sequencing revealed that the patient is a compound heterozygote. One of the mutations (a T insertion between bases 346 and 347) has been encountered before, but the second (a G-to-A substitution at base 1356) has not been previously reported. Possible explanations for the unexpected rarity of 2,8-dihydroxyadenine urolithiasis are discussed.
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keywords = nephrolithiasis
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17/19. Autosomal dominant polycystic kidney disease.

    Autosomal dominant polycystic kidney disease (ADPKD) is an important cause of medical morbidity in the united states that affects one-half million persons and accounts for ESRD in about 10% of the chronic dialysis population. In addition to its effects on the kidney, the disease has important manifestations in the cardiovascular system (aneurysms, hypertension) and the gastrointestinal tract (hepatic cysts). Clinically important renal complications can develop as the disease progresses that require specialized attention, such as urinary tract infection, pain, and nephrolithiasis. The underlying cellular defect that causes ADPKD has eluded investigators thus far, but abnormalities in cellular proliferation, the tubular basement membrane, and cell fluid secretion appear important in pathogenesis. Factors that mediate progressive interstitial fibrosis and failure of renal function are undefined, although rigorous control of blood pressure appears to be an important therapeutic measure. Recent advances in molecular biology have localized the abnormal gene to chromosome 16 in 90% of families, making early genetic screening of asymptomatic family members possible in many cases. A positive diagnosis may have important effects on employment status, as well as health insurance, so that family members sometimes refuse to be assessed for the presence of the disease. Because of such complex social factors, counseling of an asymptomatic individual by his or her physician is required when considering the use of screening tests for ADPKD. Inadequate patient education may still represent an impediment to early detection, genetic counseling, and timely treatment of disease complications.
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18/19. Detection of primary hyperoxaluria type 2 (L-glyceric aciduria) in patients with maintained renal function or end-stage renal failure.

    Primary hyperoxaluria (PH) type 1 and type 2 are autosomal recessive defects of oxalate metabolism resulting from glyoxylate accumulation which occurs by two distinct pathways. PH1 is associated to glycolic aciduria; PH2 to L-glyceric aciduria. Because hyperoxaluria leads to nephrolithiasis or nephrocalcinosis in both, they can be differentiated only through detection of the associated acidurias. However, glycolate and L-glycerate assays are not widely available and, in the setting of ESRF, diagnosis is hampered by a number of misleading events. At any stage of the disease diagnosis is crucial because there are differences between the two forms in clinical behaviour, long-term prognosis, and treatment. In this paper we outline diagnostic criteria for identification of PH2 in two patients, one with maintained renal function and one with ESRF on CPD, based on the use of a novel HPLC assay of L-glycerate in different body fluids. With the routine application of this procedure PH2 has been identified in two of 23 patients fulfilling criteria for diagnosis of PH. This suggests that the type 2 variant of PH may occur more frequently than so far suspected, and should be tested for even in the setting of ESRF.
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19/19. indinavir nephropathy in an AIDS patient with renal insufficiency and pyuria.

    indinavir has been described to cause crystalluria and nephrolithiasis in a variable number of treated patients. Acute renal failure, often reversible with discontinuation of the medication, induction of a diuresis and correction of urinary obstruction if present, occurs in a smaller percent of patients. One recent report described renal biopsy findings, indinavir crystals within cellular casts in the collecting tubules, in a patient receiving this antiretroviral agent. We report a second case of a patient with mild renal insufficiency and pyuria following indinavir therapy and describe similar renal biopsy findings.
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