Cases reported "Kidney Diseases"

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1/69. Irreversible glomerular lesions induced by crystal precipitation in a renal transplant after foscarnet therapy for cytomegalovirus infection.

    AIMS: foscarnet is an antiviral agent used to treat cytomegalovirus infection in AIDS patients and in transplant recipients. In most cases, foscarnet induces reversible tubulo-interstitial lesions which can be avoided by correct hydration. We report the first case of crystal foscarnet precipitation within glomerular capillaries in a renal transplant. methods AND RESULTS: The recipient, a 49-year-old man, developed a nephrotic syndrome with haematuria and an acute renal failure after foscarnet therapy for cytomegalovirus (CMV) infection. The polarization examination of the first graft biopsy revealed the presence of birefringent crystals within glomeruli and tubules. Infrared analysis attested to the presence of trisodium foscarnet salts and mixed sodium calcium salts coloured by Von Kossa's reaction. A second biopsy showed glomerular sclerosis, interstitial fibrosis, tubular atrophy and crystal vanishing. polymerase chain reaction (PCR) in situ applied to this biopsy confirmed the diagnosis of cytomegalovirus infection. CONCLUSIONS: These adverse effects might be the result of a toxic synergy between foscarnet and other drugs. In cases with crystalline precipitation, graft biopsy remains the best mean of diagnosis and follow-up of glomerular damage.
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2/69. bk virus renal infection in a patient with the acquired immunodeficiency syndrome.

    BACKGROUND: We describe herein a patient with the acquired immunodeficiency syndrome and renal failure due to biopsy-proven bk virus (BKV) infection. Three months after the diagnosis of the renal viral infection, his condition remained unchanged. Although BKV has previously been shown to be associated with ureteral stenosis and renal damage in renal transplant patients, to our knowledge, the literature contains only 3 cases describing the presence of BKV lesions in the kidneys of immunosuppressed patients who had not undergone transplantation. methods: The presence of BKV infection was demonstrated by means of histology, immunohistochemistry with polyclonal anti-SV40 antibody, immunoelectron microscopy, polymerase chain reaction, and enzymatic cleavage with BamHI. RESULTS: Histologic examination revealed interstitial inflammatory infiltrates and tubules with enlarged and eosinophilic nuclei. CONCLUSIONS: The high frequency of latent BKV infection and its reactivation during immunosuppression suggest that the possibility of its involvement in renal damage should be considered in immunocompromised patients.
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3/69. kidney involvement in a 17-year-old boy with eosinophilic fasciitis.

    Eosinophilic fasciitis (EF) is characterized by symmetrical scleroderma-like induration of skin over one or more distal extremities, peripheral eosinophilia, absence of Raynaud phenomenon and visceral involvement and a favourable response to systemically administered corticosteroids. Like other scleroderma-like disorders EF is rarely described in children. We report renal involvement in a 17-year-old boy with EF. urinalysis disclosed proteinuria. Prior to corticosteroid therapy renal biopsy was performed which revealed ischemic collapse of glomerular capillaries and atrophy of tubules of the cortex. Electron-microscopic studies showed hyperplasia of the renin-producing epitheloid cells in the juxtaglomerular apparatus. Few other publications have depicted renal involvement in EF of quite different character. In these cases renal biopsy and histological classification is warranted because of prognostic and therapeutic implications.
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4/69. Leukemic urate nephropathy.

    The tubules appear to be the primary sites of injury in renal failure and urate nephropathy associated with leukemia. Tubular injury is not always associated with precipitation and phagocytosis of crystals, except in the collecting tubules where cellular changes are invariably caused by intraluminal crystallization of urates. The electron microscopical observations in this communication may apply to the urate nephropathy associated with hyperuricemia of various causes.
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5/69. Reemergence of sucrose nephropathy: acute renal failure caused by high-dose intravenous immune globulin therapy.

    sucrose nephropathy was first described more than 50 years ago. The disorder is characterized by acute renal failure caused by the uptake of sucrose by renal proximal tubule cells with subsequent cellular swelling and occlusion of the tubule lumen. Approximately 114 cases of renal failure have been associated with high-dose intravenous immune globulin (IVIG) therapy. Almost all cases were caused by preparations containing large amounts of sucrose. Clinicians should consider using IVIG preparations containing no sucrose in patients who are at high risk for renal failure. risk factors include older age, baseline renal failure, and volume contraction.
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6/69. Immunotactoid glomerulopathy characterized by steroid-responsive massive subendothelial deposition.

    We report a case of immunotactoid glomerulopathy with unique histologic findings in serial biopsies. A 73-year-old man complained of developing general edema. Laboratory data on admission presented moderate renal dysfunction with nephrotic syndrome. There was no evidence of systemic disease that might cause secondary glomerulopathy. light microscopy of the renal specimen revealed lobulation of glomerular tufts and massive endothelial deposition of hyaline-like periodic acid-Schiff-positive substance with neutrophilic infiltration. The deposits were positive for immunoglobulin by immunohistochemical stains but negative for Congo red stain. Electron microscopy disclosed the deposition of microtubular structure (60 nm in diameter) predominantly in the subendothelial area and to some extent in the subepithelial and mesangial areas. Some of the tubules were extremely large (100 to 130 nm in diameter) and displayed a unique scroll structure in cross-section. The patient was treated with two sessions of plasma exchange and subsequent oral prednisolone (30 mg/d). proteinuria and renal dysfunction improved significantly in the following 2 months. Second and third renal biopsies revealed disappearance of the deposit along with the improvement of proteinuria and renal dysfunction. Because similar microtubular structures were found in neutrophils in the glomerulus as well as in the urinary sediment, phagocytosis was suggested as a possible mechanism for removal of the deposit.
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7/69. Gitelman's syndrome (familial hypokalemia-hypomagnesemia).

    Gitelman's syndrome (GS) is a heritable renal disorder characterized by hypomagnesemia, hypokalemia and hypocalciuria, and distinct from Bartter's syndrome (BS). As compared to those with BS, patients with GS present at an older age, and they have a milder clinical picture, normal or slightly decreased concentrating ability, reduced urinary excretion of calcium, and permanently decreased serum magnesium level. GS is caused by defective NaCl transport in the distal convoluted tubule, and linked to the gene encoding the thiazide sensitive Na-Cl-cotransporter located on chromosome 16q. patients with BS, on the other hand, have mutations in the transporters in the thick ascending loop of henle (NKCC2, ROMK, and C1C-Kb). Treatment of GS consists of magnesium salt replacement. Long term prognosis in terms of maintaining growth, preserving renal function and life expectancy is excellent.
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8/69. azoospermia due to testicular amyloidosis in a patient with familial mediterranean fever.

    We describe a patient suffering from familial mediterranean fever (FMF) who presented to our clinic with secondary infertility of 2 years due to amyloid A amyloidosis. His spermiogram disclosed azoospermia. A testicular biopsy revealed hyalinized tubules devoid of full spermatogenesis and containing abundant amyloid, confirmed by congo red stain. We suggest that testicular amyloidosis be taken into consideration when dealing with azoospermic FMF patients. In view of the progressive nature of amyloid accumulation in the testis we propose to follow routinely the spermiogram of FMF patients with renal amyloidosis. Furthermore, consideration of sperm cryopreservation is suggested in these cases. In FMF patients with azoospermia consideration of testicular biopsy is recommended as early as possible in order to increase the chance of sperm retrieval.
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9/69. Galloway-Mowat syndrome: a glomerular basement membrane disorder?

    We report a female infant with Galloway-Mowat syndrome. In addition to the characteristic dysmorphic appearance, neurological anomalies and early-onset nephrotic syndrome, she had arachnodactyly, an observation thus far reported uniquely in taiwan. Also, her elder sister had the same condition. Renal pathology on light microscopy showed cystic dilatation of the renal tubules. Electron microscopy showed an irregular glomerular basement membrane and effacement of foot processes. This observation suggests that malformation of the glomerular basement membrane may cause the glomerulopathy in Galloway-Mowat syndrome.
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10/69. Hepatocyte nuclear factor-1beta: a new kindred with renal cysts and diabetes and gene expression in normal human development.

    The hepatocyte nuclear factor-1beta (HNF-1beta) transcription factor controls endoderm development. Human mutations cause early-onset diabetes mellitus and have recently been associated with dysplastic, hypoplastic, and glomerulocystic kidneys. A new kindred with this "renal cysts and diabetes" syndrome is described, and nephrogenic HNF-1beta expression is defined. The proband had congenital cystic kidneys: over the next 12 yr, his renal function was impaired, but he was normoglycemic. His mother developed diabetes during pregnancy: renal ultrasonography at age 24 yr was normal, but she subsequently developed cysts. Both subjects have a heterozygous frameshift mutation in HNF-1beta that results from a 1-bp insertion in exon 5 (Y352fsinsA). When reverse-transcription PCR and in situ hybridization were used, HNF-1beta mRNA was detected in normal human metanephroi, with the highest levels of transcripts localized to fetal medullary and cortical collecting ducts and low levels of expression in nephrogenic cortex mesenchyme, primitive nephron tubules, and immature glomeruli. These results constitute the first demonstration of HNF-1beta expression during human nephrogenesis and emphasize a disease spectrum associated with HNF-1beta mutation.
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