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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This investigation was initiated to study and correlate the clinical and ultrastructural aspects of glomerulonephritis induced in the laboratory mouse by the intraperitoneal injection of a sublethal dose of murine cytomegalovirus. An attempt was made to ascertain the pathogenesis of the glomerular changes and the resultant viremia. Murine cytomegalovirus infection caused an acute transient glomerulonephritis in young female mice of the HA/ICR strain. Mice that survived a sublethal inoculation of homogenized infected gland developed transient proteinuria and excreted tubular casts. The murine cytomegalovirus infection resulted in a glomerular lesion that was selective for the mesangial cell. After entering the mesangial cell by phagocytosis the virus replicated in the nucleus and was excreted into the channel of the mesangial matrix, with extension toward the periphery of the capillary loop and adjacent to the urinary space. Virus particles were rarely found in the glomerulus after the 5th day of infection and chronic renal disease was not observed.
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PMID:Murine cytomegalovirus glomerulonephritis: clinical and ultrastructural observations. 18 Aug 54

Histologic and immunopathologic studies were performed at autopsy on the kidneys of a patient in whom hematuria and proteinuria developed in association with cytomegalovirus (CMV) pneumonitis. Light microscopic examination of the kidneys revealed focal mesangial proliferative glomerulonephritis. Immunofluorescent microscopy revealed a granular deposition of IgG, IgA, C3, and C4, mainly in the mesangium. CMV antigens were also demonstrated in a similar immunofluorescent pattern. Glomerulus-bound immunoglobulins were eluted and demonstrated to contain antibodies to CMV antigens. These findings suggest that in some patients who have CMV infection immune-complex glomerulonephritis is induced by glomerular deposition of CMV antigen-antibody complexes.
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PMID:Immune-complex glomerulonephritis associated with cytomegalovirus infection. 22 31

Ten patients with acquired immunodeficiency syndrome with newly diagnosed cytomegalovirus (CMV) retinitis were treated with an induction regimen of intravenous foscarnet, 60 mg/kg of body weight, administered as a 2-h infusion and repeated every 8 h for 14 days. At the end of induction, 9 of 10 patients had stabilized (no new retinal lesions and stable old lesions [7 patients]) or improved (decreased retinal opacification [2 patients]). All eight patients with CMV in urine or blood upon entry into the study had negative urine and blood cultures at the end of induction. After induction therapy, seven patients continued maintenance foscarnet therapy, 60 mg/kg as a single daily infusion, 5 days/week. In six patients, retinal lesions increased in size after 2 to 32 weeks of maintenance therapy. One was invaluable because a retinal detachment developed. Only 9 of 42 blood and urine cultures obtained during maintenance foscarnet therapy yielded CMV, compared with 7 of 14 obtained prior to the initiation of foscarnet induction therapy (P = 0.04). Foscarnet toxicity was mild and infrequent: elevation in serum creatinine by 0.5 to 1.3 mg/dl over the base line (two patients), muscle twitching (three patients), hemoglobin decrease by 1 mg/dl (two patients), nausea (two patients), absolute neutrophil count decrease by 50% (one patient), rise in serum phosphorus to greater than 5.5 mg/dl (four patients), and proteinuria (two patients). Intermittently administered intravenous foscarnet appears to be an effective, relatively nontoxic therapy for CMV retinitis. Additional studies to determine the optimal dosage for maintenance therapy are needed, as are comparative trials with ganciclovir.
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PMID:Foscarnet treatment of cytomegalovirus retinitis in patients with the acquired immunodeficiency syndrome. 254 90

Four previously healthy children presented in a 6-week period with marked hypoproteinemia without liver disease, malnutrition, or significant proteinuria. They all had strikingly similar radiographic findings consisting of enlarged folds confined to the fundus and body of the stomach. Three of the children had prodromal symptoms suggesting a viral illness. Cytomegalovirus was cultured from the urine in all cases and from the gastric biopsy specimens in three patients. Two of these patients also showed intranuclear inclusions in their biopsy specimens compatible with cytomegalovirus. It is not certain if cytomegalovirus was the cause of the illness.
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PMID:Pediatric hypertrophic gastropathy. 302 Sep 54

To study the effectiveness and nephrotoxic side-effects of cyclosporin A (CsA) in renal transplant recipients, a prospective randomised trial was designed to compare CsA with azathioprine (Aza). Each treatment group consisted of 40 patients; in the CsA group, 18 were randomly selected for conversion to Aza after 3 months. The 1-year graft survival for CsA-treated patients was 87% compared with 66% for the Aza group (P = 0.033). Anti-rejection therapy was administrated to 78% of the patients in the Aza group and 47% of those in the CsA group (P less than 0.01). There was no difference in the incidence of primary non-functioning kidneys, cytomegalovirus infections, hypertension, or degree of proteinuria between the two treatment groups. At 3 months the mean creatinine clearance was 42 +/- 2 ml/min (mean +/- SEM) for the CsA group compared with 56 +/- 4 ml/min for the Aza group (P less than 0.01), whereas the mean creatinine clearances at 6 months for both the converted and the non-converted CsA-treated patients did not differ from that found in the Aza-treated group. At 1 year, the mean creatinine clearance for CsA-treated patients who were converted to Aza was higher than that found for Aza-treated patients (62 +/- 7 vs 50 +/- 6 ml/min; P less than 0.05). Furthermore, the increment in creatinine clearance observed after conversion from CsA to Aza at 3 months showed a linear relationship (r = 0.9061) with the CsA trough levels before discontinuation of the drug. This indicates that CsA treatment induces a dose-dependent, nephrotoxic side-effect which is probably reversible.
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PMID:A prospective randomised comparative study on the influence of cyclosporin and azathioprine on renal allograft survival and function. 311 Jun 62

A retrospective analysis of 60 patients with Acquired Immune Deficiency Syndrome (AIDS) seen between 1981-1985 was performed to determine the genitourinary manifestations of this disease. Twenty-two per cent were found to have significant proteinuria, while 7 per cent had nephrotic syndrome which was associated with an extremely rapid demise. Renal insufficiency occurred in 27 per cent and renal biopsy results, when abnormal, revealed focal and segmental glomerulosclerosis. Pyuria was found in 52 per cent of patients, and urinary tract infections occurred in 20 per cent. Atypical pathogens including Candida, Salmonella, Acinetobacter calcoaticus, and cytomegalovirus were encountered.
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PMID:Urologic manifestations of AIDS. 367 77

Four patients (2 were HBsAg positive) with acute icteric viral hepatitis (VH) developed acute renal failure (ARF) in the course of their illness and in the absence of other complications. Their peak serum creatinine values (4.7-10, mean 7 mg/dl) were reached either before or simultaneously with their maximum serum aminotransferase values (1,390-2730, mean 2,032 mU/ml). Apart from VH no other factors responsible for precipitating ARF could be identified. In the HBsAg-negative patients, serological investigations for infectious mononucleosis, cytomegalovirus infection, and leptospirosis were negative. In 2 patients liver biopsy showed changes consistent with VH. Proteinuria was absent in all cases, making glomerulonephritis unlikely. The urinary sodium excretion was uniformly high (57-104, mean 78 mmol/l in random samples). Two patients required short courses of dialysis. All cases recovered completely with return of serum creatinine to normal values after a mean duration of 25 days. After a normal serum creatinine level had been achieved, 1 case was lost to follow-up, and the other 3 cases maintain normal renal and liver function tests 9 months (mean) after the initial episode. Otherwise uncomplicated VH is a potential cause of ARF, even in the absence of severe hepatic insufficiency. The mechanism of ARF in VH is unknown, but vasoconstriction phenomena induced by endotoxemia might contribute.
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PMID:Acute renal failure complicating viral hepatitis in the absence of severe hepatic insufficiency. 406 5

HA/ICR mice injected intraperitoneally with an LD(10) of murine cytomegalovirus develop a transiet acute glomerulonephritis characterized by cytomegalic intranuclear inclusions limited to mesangial cells. Viruria and proteinuria occur on the 3rd day and usually subside by the 10th day, accompanied by resolution of the glomerular lesion. By electron microscopy, virus synthesized within mesangial cell nuclei accumulates in intercelluar channels that course through the mesangial matrix. Virus and cellular debris are also found in channels surrounded by matrix in the juxtaglomerular area and between the epithelial cells of the macula densa. By immunofluorescence, viral antigen first concentrated in glomerular mesangial cells on the 5th day is cleared centripetally, appearing as fine granules in the juxtaglomerular area by the 7th day after infection. By the 10th day, changes are restricted to the juxtaglomerular region, and thereafter hyalinization at the glomerular vascular pole or cellular disarray of the juxtaglomerular zone with lymphocytic infiltration extending into the renal interstitium from few glomeruli occurs in approximately 40 per cent of the mice associated with persistence of viral antigen in these foci. These findings indicate that at least one route of transport resulting in viruria involves the glomerular mesangium, juxtaglomerular zone, and the distal convoluted tubule. Persistence of viral antigen or other noxious substances along this route may result in a unique juxtaglomerular lesion and interstital nephritis.
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PMID:Acute cytomegalovirus glomerulonephritis: an experimental model. 624 73

Renal biopsy was performed in 20 graft recipients to characterise the histological features associated with poor renal function concomitant with cytomegalovirus infection (CMV). Eight patients presented with proteinuria, three had microscopic haematuria at onset, and five were hypertensive. Infection was accompanied by clinical symptoms (fever, leucopenia, mild hepatic damage, or pneumonitis) in 15 patients. In all cases, serum creatinine was greater than 2 mg/dl. All patients showed some glomerular alteration on biopsy, and vascular changes were the predominant feature in seven cases. IgM and complement (C3) were found in the glomeruli of five of six patients studied by immunofluorescence. Serum creatinine was below 2 mg/dl at ten to 26 months following the infectious episode in four patients and between 2-3 mg/dl in three patients. The remaining 13 developed irreversible rejection and end-stage renal failure. We conclude that CMV, the most commonly recognised viral infection following transplantation, can cause renal changes, both glomerular (CMV glomerulopathy) and vascular (transplant vasculopathy), which may induce poor graft function.
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PMID:Renal changes in cytomegalovirus infection. 630 1

Although acute infection with murine cytomegalovirus (MCMV) resulted in a transient focal glomerulonephritis characterized by mesangial inclusions, infection of HA/ICR mice given antilymphocyte globulin (ALG) led to progressive glomerulonephritis and renal failure. ALG alone without virus failed to produce progressive renal disease. Mice given both MCMV and ALG developed severe proteinuria and azotemia with glomerular crescents by 30 days. By immunofluorescence, viral antigen was limited to mesangial zones and glomerular axial poles. Granular deposits of rabbit IgG from ALG, mouse IgG, and C3 along the peripheral glomerular capillary walls were first observed 12 days after infection. By electron microscopy, virus was found only in glomerular mesangial cells that resembled macrophages. Intramembranous and subepithelial deposits in peripheral capillary walls were associated with accumulations of polymorphonuclear leukocytes dissecting into glomerular basement membranes. These observations best fit a multiphasic mechanism of glomerular injury initiated by persistent virus in the mesangium, followed by deposits of rabbit IgG from ALG, mouse IgG, and C in the peripheral capillary walls, resulting in an amplified immune-complex-mediated injury. Because other viruses localize within the glomerular mesangium, viruses should be considered potential causes of mesangial injury and progressive glomerulonephritis.
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PMID:Progressive cytomegalovirus glomerulonephritis - An experimental model. 631 Oct 18


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