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)

To provide information on the possible influence that hypertension or its treatment might have on the development of cysts in autosomal dominant polycystic kidney disease, we studied the effects of the sodium content of the diet, DOCA-salt hypertension, renovascular hypertension, and the administration of enalapril or furosemide on the development of 2-amino-4-5-diphenylthiazole (DPT)-induced renal cystic disease. DOCA-salt hypertension caused vascular and glomerular lesions and proteinuria, but it did not enhance the development of cysts. Cytogenesis was enhanced in experimental conditions where the renin-angiotensin system is known to be activated. On the other hand, interventions known to suppress the renin-angiotensin system lessened the development of cysts. We hypothesize that this effect might be mediated by intrarenal angiotensin II and its capacity to promote cell growth and to control the postglomerular vascular resistances and the compliance of the renal interstitium.
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PMID:Mechanisms affecting the development of renal cystic disease induced by diphenylthiazole. 284 32

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

The effects of hypertension on the course of early chronic renal failure were evaluated in 233 patients with renal disease of diverse etiology, followed for 12-166 months (mean 51.35) on protein-restricted diet. On entry, 174 patients (74.6%) were hypertensive and 59 (25.4%) were normotensive. Serum creatinine levels rose from 2.40 +/- 1.11 to 4.84 +/- 3.26 mg/dl in the overall population. Deterioration of renal function was more evident in hypertensives (percent increase in serum creatinine 112.8, monthly increase 0.053 mg/dl) than in normotensives (percent increase 70.9, monthly increase 0.032 mg/dl). This difference, however, was not statistically significant. Progression of renal failure was significantly faster in hypertensive than in normotensive patients in the groups of polycystic kidney disease and chronic renal failure of unknown etiology. The actuarial renal survival probability at 72 months was 77% in normotensives and 47% in hypertensives. Among the 84 patients (36.1%) who had a fast deterioration of renal failure, 71 (84.5%) were hypertensive. In conclusion, hypertension seems to play an important role in worsening the prognosis of patients with renal parenchymal disease and early chronic renal failure. It is still difficult to separate the exact role of hypertension from the constellation of pathogenetic factors (such as the underlying renal disease, the magnitude and duration of proteinuria, the inadequate dietary contents of protein and phosphate) which may affect the progression of chronic renal disease in man.
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PMID:Role of hypertension on the progression of renal disease in man. 320 72

We report a patient with polycystic kidney disease, advanced renal failure, and nephrotic-range proteinuria. Kidney biopsy revealed IgA nephropathy with lesions of focal and segmental glomerular sclerosis. This association had not been previously described and is probably coincidental. This case supports the assumption that the nephrotic-range proteinuria observed in some polycystic patients could be the consequence of another superimposed glomerular disease. This glomerulopathy can worsen the course of azotemia in these patients.
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PMID:IgA nephropathy and polycystic kidney disease. 321 62

Chronic (30 weeks) structural and functional changes were correlated in diphenylthiazole (DPT)-induced polycystic kidney disease (PKD) in rats. DPT induced two different types of progressive tubular changes: cystic transformation and hyperplastic/atrophic tubular changes. Cystic changes diffusely involved collecting tubules in the outer medulla and cortex, and they were progressive over 30 weeks. Hyperplastic/atrophic changes occurred as clusters of tubules in the cortex and involved between 25% and 50% of tubular profiles after 12 and 30 weeks of drug treatment. Thus, the two types of tubular change were independent of each other and represent different cellular responses to the drug. DPT treatment induced no detectable light- and electron-microscopic or histochemical alterations in glomeruli or renal blood vessels. Renal functional changes consisted of: (1) early (4 weeks) and persistent impairment of concentrating ability; (2) a progressive drop in creatinine clearance and elevation in BUN; and (3) the late onset (30 weeks) of moderate proteinuria. These findings suggest that cystic as well as hyperplastic-atrophic tubular changes contribute to the loss of tubular and renal function in DPT-induced PKD. Both types of tubular lesions may have a role in the development of impaired renal function in other forms of experimental and clinical PKD.
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PMID:Renal functional changes in experimental cystic disease are tubular in origin. 335 61

Urinary doubly refractile lipid bodies (DRLB) are a characteristic finding in patients with glomerular renal diseases causing heavy proteinuria. DRLB are felt to be an uncommon finding in glomerular diseases without heavy proteinuria, and a rare finding in nonglomerular renal diseases. In order to determine whether DRLB are found in nonglomerular renal diseases, we reviewed the medical records of all patients who had urinalyses performed in our laboratory from February 1975 to June 1983. Three hundred sixty one patients demonstrated less than or equal to +2 proteinuria, and at least two DRLB. Of these, 290 were identified as having a single renal diagnosis. One hundred forty eight patients (51%) had a variety of acute and chronic glomerular diseases, and 125 patients (43.2%) had nonglomerular renal diseases, including acute tubular necrosis (ATN), prerenal azotemia, chronic interstitial nephritis, polycystic kidney disease, acute interstitial nephritis, renal neoplasia, and acute myeloma kidney. Ten patients had transient proteinuria associated with acute illness, and seven patients had no renal disease at all. Only two patients with nonglomerular renal disease had more than five DRLB per 20 high power microscopic fields. The frequency of DRLB in patients with nonglomerular renal diseases was: chronic interstitial nephritis, 26%; polycystic kidney disease, 38%; prerenal azotemia, 20%; ATN, 15%; and acute interstitial nephritis, 33%. These data suggest that at lower levels of proteinuria, DRLB are found frequently in nonglomerular renal diseases, and that DRLB do not differentiate glomerular from nonglomerular renal diseases unless more than five DRLB are found on urinary sediment examination.
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PMID:Urinary doubly refractile lipid bodies in nonglomerular renal diseases. 335 69

A case of renal angiomyolipoma originating from polycystic kidney with horseshoe kidney is reported. A 32-year-old woman visited our hospital with the complaint of proteinuria. with computerized tomographic scan and further examinations the patient was diagnosed as having renal angiomyolipoma with tuberous sclerosis. The tumor originated from a polycystic horseshoe kidney. Three weeks later, she complained of right flank pain and was diagnosed with spontaneous rupture of the angiomyolipoma. Right heminephrectomy was performed and histological examination confirmed the preoperative diagnosis. Some discussion is made on the characteristics and treatment of renal angiomyolipoma, and the statistics on renal diseases with tuberous sclerosis in Japan are presented.
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PMID:[A case of angiomyolipoma originating from polycystic kidney with horseshoe kidney]. 343 97

Urinary doubly refractile lipid bodies (oval fat bodies) are observed most frequently in patients with heavy proteinuria resulting from glomerular disease. We observed doubly refractile lipid bodies (DRLB) in the urine sediment of 60% of 35 patients with autosomal dominant polycystic kidney disease (ADPKD). All patients had clinical courses typical of ADPKD, and none exhibited the features of a second, unrelated renal disease. DRLB in the urine were correlated with a urine dipstick protein reading exceeding trace. Age, sex, BP, and serum creatinine concentration were not associated with the presence of DRLB in the urine. Examination of cyst fluid obtained from kidneys of six ADPKD patients revealed DRLB in 80% of cyst fluid samples that contained degraded blood (so-called chocolate cysts). The DRLB in cyst fluid were morphologically indistinguishable from those observed in urine, and DRLB from both sources were stained with oil red O. We conclude that urinary DRLB are a clinical feature of ADPKD.
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PMID:Urinary lipid bodies in polycystic kidney disease. 396 70

The urinary excretion of beta-hexosaminidase in relation to creatinine was studied during one year in 30 consecutive patients with polycystic kidney disease (S-creatinine 75-1 000 micro mol/l) and 30 healthy controls. The excretion of beta-hexosaminidase was significantly increased in the patients and was positively correlated to S-creatinine and to the relative increase in S-creatinine during the year of the study. No correlation was found between the enzyme excretion and age, mean blood pressure, number of antihypertensive drugs, proteinuria or pyuria. A significant rise in beta-hexosaminidase excretion was observed in two patients with acute cyst bleeding and/or kidney infarction.
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PMID:Urinary beta-hexosaminidase excretion in polycystic kidney disease. 646 Apr 26

Urinary Tamm-Horsfall glycoprotein (TH) excretion was measured by radioimmunoassay in 98 patients (55 men), aged 43.8 +/- 13.5 years, with renal disease. The radioimmunoassay was not affected by the urinary protein concentrations encountered. TH excretion (19 +/- 18 mg/24 h) was significantly lower than that in normals (39 +/- 13 mg/24 h; p less than 0.001) and was not related to age, sex or urine volume (1867 +/- 848 ml). TH excretion was not influenced directly by the degree of proteinuria (0.1-20.3 g/24 h), nor by variations in proteinuria with changes in disease activity or albumin infusions. There was a positive correlation between TH excretion and creatinine clearance less than 80 ml/min (r = 0.69, p less than 0.001). Patients with polycystic kidney disease had a disproportionate reduction in TH excretion with reduction in creatinine clearance. A major factor for the lessened excretion of TH in renal disease is probably a reduction in the number of functional distal tubular cells.
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PMID:Excretion of Tamm-Horsfall glycoprotein in renal disease. 651 75


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