Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as controls. Despite equivalent cardiac performance, GFR in those treated with CsA was depressed, 47 +/- 3 versus 94 +/- 4 ml/min/1.73 m2 (P less than 0.001). CsA therapy was also associated with significant elevation of renal vascular resistance (RVR), proteinuria, arterial hypertension, and impaired intrarenal conversion of inactive prorenin to active renin. Histopathological changes associated with CsA included an obliterative arteriolopathy with deposition of proteinaceous material in necrotic arteriolar walls, and associated tubulointerstitial damage. A minority of glomeruli exhibited either ischemic collapse or sclerosis. Area perimeter analysis revealed enlargement of the remaining glomeruli with significant expansion of the mesangium. Longitudinal examination over a 48 month period (N = 15) during which CsA was reduced in dosage or withdrawn revealed persistent hypofiltration, increasingly elevated RVR and heavier proteinuria. Further histopathological deterioration was observed when renal tissue was sampled a second time in six patients, and three members of the experimental group developed end-stage renal disease. We conclude that continuous CsA therapy for more than 12 months causes a chronic injury to renal microvessels that is rarely reversible and potentially progressive.
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PMID:The long-term course of cyclosporine-associated chronic nephropathy. 328 2

We followed renal function through the natriuretic phase of 6 occasions of drug-induced recovery from minimal lesions nephrotic syndrome (MLNS). Protein excretion started to fall 1-3 days prior to the start of the natriuresis. The natriuresis was accompanied by a rise in glomerular filtration rate (GFR, inulin clearance). The filtration fraction, calculated from the GFR and the p-aminohippurate clearance, rose steadily in 5 subjects in whom it was low before therapy. Proximal and distal sodium reabsorption fractions, estimated from the changes in maximum free water clearance, fell, and fractional sodium, lithium, uric acid and free water clearance rose. At the time of these changes plasma protein had hardly risen, whereas renin activity was down. These results are in agreement with the notion that the sodium retention of MLNS is due to a renal defect. Repair of the glomerular filter, evident from the disappearance of proteinuria and the rise in filtration fraction, apparently normalizes the elevated tubular sodium reabsorption proximal to the macula densa, which leads to a fall in renin release.
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PMID:Renal function during recovery from minimal lesions nephrotic syndrome. 331 90

The clinical presentation, initial laboratory and renal biopsy findings, and subsequent clinical course in 205 children with IgA nephropathy were studied retrospectively. The findings in the 119 patients with macroscopic hematuria and those in the 86 without macroscopic hematuria were compared. There were no differences with regard to sex distribution, age at onset, initial renal function, incidence of hypertension, degree of proteinuria and degree of mesangial proliferation. At the latest follow-up, 3% of the patients with macroscopic hematuria and 8% without macroscopic hematuria had developed chronic renal failure; 8% of the patients with macroscopic hematuria and 20% without had heavy proteinuria with or without hypertension (p less than 0.01); 41% of the patients with macroscopic hematuria and 24% without macroscopic hematuria had normal urine, blood pressure and GFR (p less than 0.05). The disease appears to follow a significantly more benign course in children with macroscopic hematuria than in those without macroscopic hematuria. These observations suggest some macroscopic hematuria-related differences in the natural history of childhood IgA nephropathy.
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PMID:Macroscopic hematuria in childhood IgA nephropathy. 342 31

Micropuncture studies in the rat have indicated that in the short term, the superimposition of pregnancy on an experimentally induced, advanced, autologous phase glomerulonephritis (GN) does not lead to any worsening of the functional or morphological changes characteristic of this disease. Indeed, pregnant rats with GN exhibit a tendency toward higher GFR and plasma flow rate than do virgin rats with this disease. In chronic studies to investigate the long-term effects on kidney function of pregnancy, normal rats undergoing five closely spaced pregnancies and lactations exhibit glomerular hemodynamics, 24-hour protein excretions, and morphology similar to those of age-matched virgins. When repetitive pregnancies are superimposed on rats with the long-term hyperfiltration stimuli of uninephrectomy plus high dietary protein feeding, no worsening of the proteinuria occurs in comparison to virgin rats subjected to the same degree of renal ablation plus high protein. Although filtration and plasma flow rates are lower in these repetitively pregnant rats as compared with virgin rats, amino acid infusion revealed substantial renal reserve in the repetitively pregnant rats. These studies show that gestational hyperfiltration does not, in and of itself, provide an adverse stimulus to the maternal kidney.
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PMID:Renal disease in gravid animal models. 355 8

The blood pressure, urinary symptoms (proteinuria, hematuria, casts), the albumin- and cholesterol concentration in the serum and the renal function (GFR, RPF) of 125 children with chronic glomerulonephritis (GN) were analysed. 76 children had only single symptoms (93% proteinuria, 33% hypertension), which indicated a GN. The serum albumin and cholesterol concentration were pathological in 43% of the patients and serum creatinine level was pathological in 20% of the children. After 6 years the individual courses of renal function demonstrated a deterioration of GFR and RPF for most of the children. It can be concluded, that the summary consideration of epidemiology, symptomatology and renal function of different glomerular lesions has only a limited application to the clinical practice.
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PMID:[Glomerulonephritis (GN) in childhood. I. Epidemiology, clinical aspects and kidney function in 125 children]. 359 Oct 33

Heymann nephritis is a rat model of glomerulonephritis with morphologic manifestations of human membranous nephropathy. This model is generated by immunizing rats with Fx1A antigen. Passive Heymann's nephritis (PHN) can be produced by the administration of anti-Fx1A antibody (anti-Fx1A Ab) (with abnormal proteinuria appearing in 5 days). Studies were designed to examine the evolution of temporal changes in protein excretion, the glomerular ultrafiltration coefficient (LpA) and morphology of glomerular capillary three and five days after induction of PHN. Glomerular hemodynamic evaluation by micropuncture in euvolemic rats with PHN revealed normal values for nephron filtration rate (SNGFR), LpA and the glomerular hydrostatic pressure gradient (delta P) at day three, but by day five the whole kidney GFR and SNGFR were decreased, delta P increased and LpA significantly reduced. Glomerular binding of anti-Fx1A Ab increased from 38 micrograms/7.6 X 10(4) glomeruli on day three to 52 micrograms on day five. Immune complex deposits evaluated by immunofluorescence and electron microscopy appeared larger and were better defined on day five than on day three. Epithelial foot process fusion was more extensive on day five than day three. The onset of increased proteinuria correlated temporally with a reduction in LpA on day five, which in turn correlated with increased antibody binding, immune deposit accumulation and fusion of epithelial cell foot processes.
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PMID:An evaluation of the development of experimental membranous nephropathy. 361 4

It has been proposed that ingestion of large amounts of dietary protein leads to sustained renal hyperperfusion and progressive glomerulosclerosis in rats. This hypothesis was tested in dogs, with 75% reduction in renal mass, maintained for 4 years on either 56, 27, or 19% dietary protein. Twelve of 21 dogs survived 4 years, and death due to renal failure was not correlated to diet. Dogs fed 56 and 27% protein had increased GFR and CPAH before and after reduction of renal mass compared to the 19% group. A pattern of deterioration of renal function, including proteinuria, was not found in any diet group. Nine of 11 dogs, fed 56, 27, or 19% protein had minimal glomerular lesions, including mesangial proliferation, GBM irregularities, adhesions, and sclerosis. Two other dogs, fed 56% protein, had more severe glomerular lesions. No significant ultrastructural differences were found in glomeruli among the three diet groups. These results do not support the hypothesis that high protein feeding had a significant adverse effect on either renal function of morphology in dogs with 75% nephrectomy.
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PMID:Long-term renal responses to high dietary protein in dogs with 75% nephrectomy. 370 9

The chronic effects of dietary protein on renal structure and function were studied in rats with normal and reduced renal mass. Control rats with two kidneys were compared with unilaterally nephrectomized rats, and with one and one-third nephrectomized rats obtained by unilateral nephrectomy and infarction of one-third of the remaining kidney. Rats at each level of renal mass were maintained on chow containing either 6% or 40% protein content. Separate cohorts of rats were studied four and eight months after ablation and institution of these dietary regimens. At both time intervals and at all levels of renal mass, rats fed the high protein diet had higher average values for GFR than comparable animals fed the low protein chow. Within each of the dietary regimens the animals with loss of renal mass developed greater prevalences of sclerotic glomeruli by eight months. Furthermore, at each level of initial renal mass, rats eating the high protein diet had a greater prevalence of sclerotic glomeruli than those on the low protein diet. Similarly, rats on the high protein diet had greater rates of protein excretion than those on the low protein diet at each degree of ablation. The prevalence of sclerosed glomeruli increased between four and eight months in each group. Thus, the extent of renal injury as manifested by proteinuria and glomerular sclerosis was directly related to the degree of initial loss of renal mass, and dietary protein restriction retarded these manifestations of injury across a wide range of initial renal mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic effects of dietary protein in the rat with intact and reduced renal mass. 378 91

Clinicopathologic correlations were examined in 75 children with focal segmental glomerulosclerosis (FSGS) associated with idiopathic nephrotic syndrome. The biopsy specimens of all patients were examined by electron microscopy (69 patients) or immunofluorescence microscopy (67 patients) in addition to light microscopy. Fifty-three patients (group A) had FSGS diagnosed on their first biopsy; 22 patients (group B) had one to three previous biopsies showing minimal glomerular changes or mesangial hypercellularity prior to the demonstration of FSGS on a subsequent biopsy. Considerable homogeneity between the diagnostic biopsy features in the two groups was evident. Diffuse mesangial hypercellularity and IgM deposition were found in a similar percentage of each group, but these features did not correlate with each other. To date, the mean duration of follow-up for the entire group has been 57 months (range, 7 to 217 months): 21% have developed ESRD, 23% have a decreased GFR but not ESRD, 37% have persistent proteinuria only, 11% are in remission, and 8% have been lost to follow-up. No morphologic or clinical features have been predictive of outcome during this relatively short period of followup. The frequency of chronic renal failure and ESRD has been similar in groups A and B. These data suggest that the clinical outcome in children with FSGS is poor in many patients, whether the diagnosis is established on an initial or subsequent renal biopsy specimen.
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PMID:Focal segmental glomerulosclerosis in children with idiopathic nephrotic syndrome. A report of the Southwest Pediatric Nephrology Study Group. 388 99

In this study, we have evaluated 50 children (30 girls and 20 boys; mean age, 10.1 years) with a variety of renal diseases in whom renal biopsy specimens showed crescents in greater than or equal to 50% of glomeruli. Initial clinical features included edema in 61%; hypertension in 51%; gross hematuria in 73%; 3 to 4+ proteinuria in 78%; and severely decreased GFR (less than 30 ml/min/1.73 m2) in 66%. When the total number of patients was divided into those with 50 to 79% crescents (N = 18) and those with 80 to 100% crescents (N = 32), no significant difference in outcome could be demonstrated, with endstage renal disease (ESRD) being seen in 44 and 52% of the two groups, respectively. Pathologic features associated with a poor prognosis included predominance of large crescents (P = 0.004) or fibrous crescents (P = 0.03); increased frequency of gaps in Bowman's capsule (P = 0.004); global glomerular sclerosis (P = 0.05); glomerular IgM (P = 0.003); interstitial fibrosis (P = 0.03); and tubular atrophy (P = 0.04). At followup, GFR was normal in all patients with poststreptococcal GN, but low in 60% of patients with other conditions. The study permits the following conclusions: (1) Approximately 50% of children with crescents in 50% or more glomeruli progress to ESRD; (2) a poor prognosis is associated with (a) a high percentage of large crescents, (b) increased frequency of gaps in Bowman's capsule, and (c) evidence of chronic histologic changes, but not with the percentage of crescents per se; and (3) the underlying type of glomerulonephritis is considered a helpful prognostic indicator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A clinico-pathologic study of crescentic glomerulonephritis in 50 children. A report of the Southwest Pediatric Nephrology Study Group. 388


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