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

Interstitial nephritis is a rare but serious adverse effect of many drugs and usually is diagnosed by clinical signs and symptoms of hematuria, proteinuria, eosinophilia, fever, azotemia, and rash. Ciprofloxacin is one drug that has been reported to cause interstitial nephritis. Renal toxicities have been reported in less than one percent of the patients receiving ciprofloxacin therapy. Limited documentation of this adverse effect exists in the literature. This article describes a patient with suspected ciprofloxacin-induced interstitial nephritis.
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PMID:Suspected ciprofloxacin-induced interstitial nephritis. 232 15

From January 1986 to December 1988, 8 patients with lupus nephritis did not respond to the administration of two courses of methylprednisolone pulse therapy and cyclophosphamide treatment for 56 days. These cases then received intravenous prostaglandin E1 (PGE1) for 3 weeks. All of them had a good response with decreased proteinuria and azotemia; serum C3 and C4 levels and creatinine clearance also increased. Both OKT4+ and OKT8+ cells increased, and the OKT4/OKT8 ratio was almost normal. The macrophage functions included increased production of interleukin 1 and gamma-interferon. The capacity to synthesize immunoglobulin after pokeweed mitogen stimulation was reduced, the circulating immune complexes lowered, and glomerular IgG deposits decreased in the two class IV follow-up biopsy cases after PGE1 therapy. These clinical improvements after PGE1 therapy are probably related to the modulation of macrophage T-B cell interaction, enhancement of reticuloendothelial system function, and increased glomerular capillary flow.
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PMID:Improvement in steroid and immunosuppressive drug resistant lupus nephritis by intravenous prostaglandin E1 therapy. 237 Sep 25

The pathogenesis, prognosis, and reversibility of renal failure were assessed in 494 consecutive, previously untreated patients with multiple myeloma. For patients with a similar extent of disease, the presence or degree of azotemia did not adversely affect prognosis. Hypercalcemia and/or Bence Jones proteinuria explained the renal failure in 97% of patients. After treatment with a combination of hydration and chemotherapy, normal renal function was achieved in 51% of patients, reversibility usually being rapid and occurring more often in those with slight elevation of serum creatinine. Myeloma control was much more important for survival prolongation than reversal of renal failure, supporting the prompt institution of effective therapy for the underlying malignancy.
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PMID:Renal failure in multiple myeloma. Pathogenesis and prognostic implications. 238 64

Complement system takes an important role in the pathogenesis of immune complex glomerulonephritis. In this study the precise changes of serum complement and its deposition in the glomeruli were investigated in the mice models induced with cationized bovine gamma-globulin (CBGG). Balb/c mice preimmunized with CBGG were injected intravenously with CBGG three times every 24 hours. Proteinuria and hypoalbuminemia have developed from day 3 until the death on day 9-13 of progressed azotemia. This nephritis resembled to mesangial proliferative glomerulonephritis histopathologically. Immunofluorescent study revealed granular deposits of CBGG, IgG, A, M and C3 along the glomerular capillary loop. Serum C3 decreased to about 50% of normal controls within 1 hour after challenge of antigen and plasma C3 conversion evaluated by crossed-immunoelectrophoresis, occurred in accordance with C3 reduction and then decreased. Immunofluorescent study showed a big difference in the mode of deposition among IgG, CBGG and C3. The most intense deposits of C3 in the glomeruli were seen 12 hours after challenge of CBGG, and then gradually decreased until the next challenge. IgG and CBGG antigen deposited most intensely soon after the challenge of antigen, and gradually decreased. These results led us to conclude that there existed two phases of complement activation in this immune complex induced mice glomerulonephritis; an early phase activation of complement by antigen-antibody complexes in the circulation and later phase activation of complement by immune complexes after deposition of them in situ glomeruli.
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PMID:[Changes of complement in immune complex glomerulonephritis induced by cationized antigen]. 253 Dec 43

Reduction of renal mass (11/12) in rats leads to progressive azotemia, proteinuria, and hypertension. Less extensive renal ablation resulting from uninephrectomy also accelerates the progression of focal glomerulosclerosis (FGS) induced by experimental diabetes, renal irradiation, aminonucleoside nephrosis, or aging. The consequence of the absence of one kidney in man are examined in three different clinical situations. Unilateral renal agenesis seems to predispose to the development of FGS, but most reports include isolated cases and the true incidence of FGS is not known. The solitary kidney following uninephrectomy for acquired unilateral disease undergoes a compensatory rise in glomerular filtration rate (GFR) that remains stable for several decades. Finally, kidney donors followed for over 2 decades show unimpaired GFR, elevated at 70% to 80% of the normal (two-kidney) GFR. Some donors develop mild, nonprogressive proteinuria. Their incidence of hypertension matches that in the control population. Thus, hyperfiltration secondary to 50% reduction of renal mass in humans does not lead to loss of function of the remaining parenchyma.
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PMID:The solitary kidney: a model of chronic hyperfiltration in humans. 277 30

Renal biopsy specimens from five patients with Takatsuki's syndrome were studied. Proteinuria and hematuria were modestly positive in four cases and three cases, respectively. One case demonstrated early azotemia, while four cases revealed normal serum creatinine levels. All cases displayed glomerular enlargement and lobulation, mesangial cell proliferation, and double contour structure, simulating membranoproliferative glomerulonephritis. It is noteworthy that mesangial loosening was also detected in the renal biopsy specimens of this study. This change was present diffuse-globally in the well-developed cases and focal-globally or segmentally in the developing cases. In addition, various morphologic expressions were observed, ie, microaneurysms congested with RBCs, tentatively termed mesangial hyaline thrombi, nodule-like lesions, and tiny to small-sized mesangiolytic lesions. Since all these features could be explained by low-grade mesangiolysis, the renal alteration associated with this syndrome was termed mesangiolytic glomerulonephritis. Humoral factor(s) also toxic to the mesangium were implicated.
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PMID:Mesangiolytic glomerulonephritis associated with Takatsuki's syndrome: an analysis of five renal biopsy specimens. 265 91

We defined a clinical staging of renal function in systemic lupus erythematosus (SLE) which uses inexpensive outpatient measures to serially stage patient status and then analyzed the disease course of 292 patients followed since 1968. The 4 mutually exclusive states used were (1) normal (creatinine less than 1.2 mg/dl and protein less than 2+ on dipstick); (2) proteinuria alone (creatinine less than 1.2 mg/dl and protein greater than or equal to 2+ on dipstick); (3) moderate filtration dysfunction (creatinine greater than or equal to 1.2 mg/dl and less than 4.0 mg/dl); and (4) severe azotemia (creatinine greater than or equal to 4.0 mg/dl). Duration in each state and subsequent transitions were incorporated in an assessment of outcome. Prognostic variables were found which predicted different outcomes within each of the 4 states. This stratification, based on renal function over time, provides a useful analytical tool for comparing subsets of patients with lupus. We found that serum complement (C3) predicted progression in state 1 and 2 as well as potential responders to therapy in state 3. No improvement was noted for patients in state 4.
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PMID:A "state model" of renal function in systemic lupus erythematosus: its value in the prediction of outcome in 292 patients. 271 6

Fifty-six patients with acute glomerulonephritis were studied prospectively during 1984. Their ages ranged from 10 months to 14 years old with the peak age range between 5 to 9 years. Most of them had edema, hypertension, hematuria with or without proteinuria and had low serum complement. Azotemia was found in 45 per cent of the cases. Serologic evidence for streptococcal infection was positive in 68 per cent and only 6 per cent had positive culture. Edema and hypertension were all resolved within 2 weeks. All patients that were followed up had normal serum complement by the 6th week, normal BUN, Scr by one year. The hematuria disappeared by 6 months and proteinuria by 2 months in 50 per cent of the cases. By the 4th year only one patient had microscopic hematuria and mild proteinuria with normal serum creatinine, normotension and no edema. In conclusion, in Thailand AGN is still a common kidney disease in children but with prompt and proper treatment its prognosis is still very good.
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PMID:Acute glomerulonephritis in children: a prospective study. 273 44

The medical records of 59 dogs with renal amyloidosis were reviewed. Most dogs with amyloidosis were greater than 6 years old, and females were affected more often than males. Beagles, Collies, and Walker Hounds were at increased risk, whereas German Shepherd Dogs and mixed-breed dogs were at decreased risk. Common historical findings were anorexia, polyuria, polydipsia, lethargy, vomiting, and weight loss. Common laboratory findings were leukocytosis, lymphopenia, nonregenerative anemia, hypercholesterolemia, azotemia, hyperphosphatemia, metabolic acidosis, isosthenuria, cylindruria, and proteinuria. Proteinuria was moderate to severe in most dogs, as assessed by qualitative determination of urine protein concentration, urine protein/urine creatinine ratio, and 24-hour urine protein excretion. Conservative medical management was of little value, and survival ranged from 3 to 20 months in 12 dogs for which this information was available. Moderate to severe diffuse global glomerular amyloidosis was detected in all dogs. Medullary amyloid deposition was multifocal and less severe, but was evident in most dogs. Secondary tubulointerstitial and glomerular lesions were mild or absent in most dogs. Thromboembolism was identified in approximately 14% of affected dogs, underlying inflammatory disease in 37%, and neoplasia in 20%. Laboratory indicators of renal function correlated poorly with histologic lesions, with the exception of glomerular amyloid deposition and "chronic renal disease" index with endogenous creatinine clearance.
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PMID:Clinicopathologic findings in dogs with renal amyloidosis: 59 cases (1976-1986). 276 63

Ischemic acute renal failure is principally a disease of the elderly, but the effect of aging on renal susceptibility to ischemic damage has not been defined. To address this issue, adolescent (3-4 months), mature (12-13 months), and aged (24-25 months) rats underwent base-line renal functional assessments, and then they were subjected to a standardized ischemic event (37-minute, bilateral renal artery occlusion). The loss of renal function [assessed by azotemia and creatinine clearance, (Ccr)] and the severity of tubular damage (necrosis, casts) were determined 24 hours later. Base-line functional assessments indicated no significant differences in Ccr/100 gm body weight between the groups, but urinary protein excretion increased with age (p less than 0.001). In response to renal artery occlusion, the adolescent, mature, and aged rats lost 59 +/- 4, 82 +/- 4, and 94 +/- 1% of their base-line Ccr (p less than 0.01), respectively. Among the proteinuric rats, no correlation was noted between percent loss Ccr and urinary protein excretion. Despite the large differences in postischemic renal function, the extent of tubular morphologic damage did not differ among the groups. The percent loss Ccr did not correlate with necrosis (r = -0.02) or casts (r = 0.07). Although focal glomerulosclerosis and mild tubular atrophy were noted in the aged kidneys these lesions were minimal to absent in the mature rats. We conclude that aging increases susceptibility to severe ischemic acute renal failure in the rat, an effect that is apparent even during a transition from the adolescent to the mature state. This finding cannot be simply ascribed to increasing proteinuria, a loss of renal functional reserve, or to increased tubular morphologic damage. The data are most consistent with the view that underlying age-related glomerular/hemodynamic changes lead to an exaggerated functional decline in response to ischemic renal injury.
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PMID:Effects of aging on expression of ischemic acute renal failure in rats. 277 Feb 46


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