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)

Exacerbation of focal sclerosing glomerulopathy (FSGN) during pregnancy was noted in the three patients. All had antecedent asymptomatic proteinuria. Toxemia developed in two of the women during pregnancy and progressed rapidly to renal failure. Severe nephrotic syndrome developed in one patient with pregnancy and remitted after delivery. These cases suggest a deleterious effect of pregnancy on the course of FSGN and indicate the necessity for doing renal biopsy in women of childbearing age with asymptomatic fixed proteinuria or nephrotic syndrome so that those patients with FSGN can be properly counseled about future pregnancies.
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PMID:Focal sclerosing glomerulopathy with adverse effects during pregnancy. 71 21

Hereditary nephritis is a disease presenting with hematuria, proteinuria, and systemic findings including ocular lesions and deafness. Renal failure frequently occurs in males who have the disease at a young age. We report the case of a female with hereditary nephritis who presented with the classic clinical and pathologic features of crescentic glomerulonephritis post-pregnancy. A sibling also had a comparable course. It is proposed that crescentic glomerulonephritis may be a heretofore unreported presentation of hereditary nephritis with terminal renal failure.
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PMID:Alport's syndrome representing as crescentic glomerulonephritis: a report of two siblings. 72 17

Chronic atrophic pyelonephritis is associated with vesicoureteric reflux in infancy. Reflux disappears during childhood in 50% of cases. It is more commonly detected in infants (49%) and children (26%) with infection than in adults (4.4%). Severe reflux may persist in adults and is usually (94%) associated with scarring. Patients with end-stage renal failure due to pyelonephritis are much younger than patients with end-stage renal failure due to other causes. The incidence of reflux according to sex is equal in infancy, but after infancy both pyelonephritic scarring and reflux are far more common in females. Infection is the likely cause of progressive scarring in females. Hypertension is associated with chronic atrophic pyelonephritis. Proteinuria is the worst prognostic feature in patients with reflux nephropathy and pyelonephritic scarring. Intrarenal reflux determines the site of scarring. The role of surgical correction of vesicoureteric reflux remains uncertain, but meticulous control of infection appears to prevent progressive scarring.
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PMID:Reflux nephropathy and chronic atrophic pyelonephritis: a review. 73 56

Antireflux surgery was performed in five patients with vesicoureteral reflux at a time when renal insufficiency was present. Notable proteinuria was present in four of the patients, and a kidney biopsy specimen showed glomerular lesions in one. Despite the eradication of reflux and of infection, all five patients continued to have progressive renal insufficiency culminating in renal failure. Vesicoureteral reflux nephropathy may include a glomerulopathy leading to progressive glomerular sclerosis. Antireflux surgery would not alter this ongoing process and therefore would not halt progressive renal failure.
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PMID:Irreversible renal failure following vesicoureteral reflux. 75 14

Six patients with mesangiocapillary glomerulonephritis and intramembranous dense "deposits" developed terminal renal failure and were transplanted, three from living and three from cadaver donors. Eight renal biopsy specimens were obtained from five of the grafts, from 1 to 26 months following transplantation. All six biopsy specimens taken later than seven months following the graft showed recurrence of dense intramembranous "deposits" in the basement membranes of glomeruli, and of Bowman's capsule and tubular basement in five. Recurrence of "deposits" was associated with deposition of C3 on immunofluorescent study in all but one specimen; in addition, IgM was found in two specimens, but IgG and early complement components were absent. Only two patients, however, showed glomerular proliferation associated with profuse proteinuria. In the other subjects the recurrence of the "deposit" was not associated with clinical findings. Graft loss, which occurred in two patients, was predominantly from rejection.
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PMID:Transplantation in mesangiocapillary glomerulonephritis with intramembranous dense "deposits": recurrence of disease. 78 88

Association of membranous glomerulonephropathy with crescentic glomerulonephritis is apparently extremely rare. We report three patients who had this combination. One patient had biopsy-proven membranous glomerulonephropathy thirteen months prior to sudden and rapid decline in renal function necessitating hemodialysis. A repeat renal biopsy showed a superimposed crescentic nephritis and antiglomerular (GBM) antibodies were demonstrable in the serum. A second patient had proteinuria of unknown duration and then developed renal failure. Renal biopsy showed crescentic nephritis with a fine granular glomerular immunofluorescence for IgG typical of membranous glomerulonephropathy. Anti-GBM antibodies were present in this patient's serum. The third patient presented with acute renal failure of moderate severity. A renal biopsy revealed crescentic nephritis, granular deposits of immunoglobulins, and epimembranous electron-dense deposits typical of membranous glomerulonephropathy. Although his creatinine clearance improved spontaneously, nephrotic syndrome has persisted and a repeat renal biopsy showed a progression of the membranous glomerulonephropathy with the disappearance of the crescentic lesions. The reason for this peculiar association of membranous glomerulonephropathy and crescentic glomerulonephritis is unclear. It is possible that deposition of immune-complexes along glomerular basement membrane may render the glomerulus more susceptible to additional injury from a variety of other agents. Alternatively, depostis formed in one disease could initiate release of normal or altered basement membrane material and lead to formation of anti-GBM antibodies and subsequent development.
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PMID:Association of crescentic glomerulonephritis with membranous glomerulonephropathy: a report of three cases. 78 51

Five patients are described in whom only gentamicin sulfate appeared responsible for acute renal failure. Subjects received 1.2 to 2.88 gm over 12 to 18 days. All were over 45 years of age, and premorbid kidney abnormalities may have enhanced susceptibility to toxic effects of the drug. Renal failure appeared 8 to 17 days after beginning gentamicin therapy and was characterized by creatinine clearances 4 to 10 ml/min, urine to plasma creatinine ratios less than 20, urinary sodium concentrations 16 to 60 mEq/liter, proteinuria, and cylindruria. Oliguria was not observed and this feature may impair recognition of kidney damage. Clinical recovery required an average of 42 days and was complete in four of five patients. Gentamicin alone may be nephrotoxic and should be given with particular caution to the elderly and those with even mild kidney abnormalities.
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PMID:Gentamicin-associated acute renal failure. 78 66

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.
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PMID:Defibrination with ancrod in nephrotoxic nephritis in rabbits. 79 57

Total serum thyroxine (T4), free thyroxine index (FTI), thyroxine binding globulin (TBG) binding capacity, serum albumin, alpha-globulins and urinary protein excretion were measured in 50 patients with chronic renal failure, but without nephrotic syndrome. 25 patients were undergoing chronic hemodialysis. T4 was within the normal range in most patients. There was a tendency to lower T4 values as compared to an age and sex-matched control group, but this did not reach statistical significance. TBG was normal in most patients. 4 patients showed elevated TBG concomitant with elevation of other alpha-globulins. Serum albumin was significantly decreased. No correlation existed between daily protein excretion and TBG or alpha-globulins, but the correlation between serum albumin and proteinuria was highly significant. T4 and proteinuria correlated with borderline significance. A highly significant correlation between T4 and TBG-albumin values was found. No correlation existed between FTI and TBG-albumin levels. The data suggest that T4 and TBG are normal in most patients with renal failure, even in the presence of significant proteinuria. Low T4 values, when found in renal insufficiency, may be secondary to low serum albumin and possibly prealbumin.
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PMID:Serum thyroxine and thyroxine-binding proteins in chronic renal failure without nephrosis. 80 56

In two patients with terminal renal failure, manifestations of disease developed in multiple organ systems. One had a previous diagnosis of multiple myeloma with kappa light chain proteinemia and proteinuria. The other had idiopathic lobular glomerulonephritis. Hepatic and neurologic abnormalities developed in both; in the latter gastrointestinal, cardiac and endocrine disease developed as well. Clinical and pathologic correlations suggest that the retention and tissue deposition of light chains produced the organ dysfunction, inasmuch as free kappa light chain determinants were demonstrated histologically in the clinically affected organs. The deposition in these patients may be an extreme example of a common but previously unrecognized form of plasma cell dyscrasia.
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PMID:Manifestations of systemic light chain deposition. 81 12


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