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)

A 5-year-old boy is presented who exhibited the classical symptoms of the syndrome described by BARTTER et al. in 1962: growth retardation, hypokalemic alkalosis, hyperplasia of the juxtaglomerular apparatus with normotensive hyperreninism-hyperaldosteronism, polydipsia with impaired renal concentration ability resistant to pitressin. In addition, the patient showed the typical proximal tubular defects of the Fanconi syndrome: hyperphosphaturia with hypophosphatemic ricktts, generalized hyperaminoaciduria, proteinuria and glucosuria. In the cases of Bartter's syndrome described to date, no uniform pathogenetic mechanism could be identified. Proximal tubular salt wasting generally is assumed to be the primary defect. The studies carried out in this case support this hypothesis and indicate that the complete clinical picture of Bartter's syndrome may occur within the framework of multiple proximal tubular defects.
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PMID:[Bartter's syndrome and tubular functional disturbances]. 115 68

A 66-year-old man with kappa-light chain multiple myeloma had adult Fanconi syndrome. Renal tubular transport abnormalities consisted of renal tubular acidosis, renal glycosuria, aminoaciduria, phosphaturia and renal hypouricemia. After therapy for multiple myeloma, urinary Bence Jones protein became undetectable, and all these renal tubular abnormalities except urate wasting were corrected. Histological examination revealed electron-dense tubular and rod-like deposits in proximal tubular epithelium. This clinical observation suggests that the renal tubular transport defects were secondary to the myeloma process, possibly due to Bence Jones proteinuria.
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PMID:Adult Fanconi syndrome secondary to kappa-light chain myeloma: improvement of tubular functions after treatment for myeloma. 211 47

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis in particular organ veins. 268 Aug 53

A 35-year-old man developed leg edema, marked hypoalbuminemia, and proteinuria. Subsequent renal biopsy revealed a diffuse membranoproliferative glomerulonephritis and, on electron microscopy, typical electron-dense deposits characteristic of an immune complex pathogenesis. Although protein wasting might have readily been explained on the basis of his nephrotic syndrome, the concomitant symptom of diarrhea led to the diagnosis of celiac sprue, another disorder with a possible immune-mediated pathogenesis. While reports of immune complex glomerulonephritis in celiac sprue are rarely recorded, the potential significance of gastrointestinal symptoms in patients with the nephrotic syndrome may have important nutritional implications, especially if underlying occult celiac sprue is recognized.
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PMID:Celiac sprue-associated immune complex glomerulonephritis. 294 90

The incidence of acute renal failure, hypertension and electrolyte disorders in 64 bone marrow transplant recipients randomized to receive either cyclosporin or cyclophosphamide was investigated. Sixty-four per cent of patients developed acute renal failure, 75 per cent hypertension, and 88 per cent significant hypomagnesemia. The incidence of diastolic hypertension and hypomagnesemia was greater in the patents treated with cyclosporin. Hypomagnesemia was due to magnesium wasting by the kidney. Both groups received similar cumulative doses of aminoglycoside antibiotics. Significant proteinuria developed in all but one patient and nephrotic-range proteinuria was noted in 21 per cent. The cause of the proteinuria is unclear; no obvious morphologic changes were seen at autopsy in patients who exhibited nephrotic-range proteinuria. The abnormalities of renal function were shown to be transient in patients who were observed for periods ranging from one to three years. It is concluded that hypertension, renal failure and hypomagnesemia are common in the setting of bone marrow transplantation. Whereas cyclosporin probably aggravates the severity of these disorders, it is likely that other factors (e.g., aminoglycoside antibiotics) play a major role as shown by the high incidence of renal and electrolyte disorders in patients treated with cyclophosphamide alone.
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PMID:Hypertension and renal dysfunction in bone marrow transplant recipients. 327 85

Renal failure in cancer patients is a common problem in oncology; this complication is frequently multifactorial in origin. Several antineoplastic agents are potentially nephrotoxic; previous renal impairment as well as combinations with other nephrotoxic drugs may increase the risk of nephrotoxicity during administration of chemotherapy. Methotrexate-related renal damage most frequently occurs with high-dose therapy and can be avoided by forced alkaline diuresis and administration of folinic acid. Renal dysfunction secondary to semustine (CH3-CCNU) is clearly related to cumulative doses in excess to 1,200 mg/m2; the onset may be delayed and renal failure progress despite drug discontinuation. Streptozotocin is also nephrotoxic and may cause proteinuria and renal tubular acidosis; progressive renal failure can be predicted by a close monitoring of proteinuria and prevented by drug discontinuance. Mitomycin-associated renal failure frequently presents with signs of microangiopathic hemolytic anemia; renal failure is usually delayed but occasionally, it may be rapidly progressive despite drug discontinuance. Cisplatin nephrotoxicity is clearly dose-related and used to be considered dose limiting. Renal insufficiency can be prevented by hydration and forced diuresis; in addition, hyperhydration with mannitol-induced saline diuresis may allow administration of high doses and thus circumvent the dose-limiting effect of cisplatin-induced renal toxicity. Cisplatin-induced renal magnesium wasting occurs frequently and should be supplemented. Other approaches to reduce cisplatin nephrotoxicity are currently under investigation and are discussed.
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PMID:Nephrotoxicity induced by cancer chemotherapy with special emphasis on cisplatin toxicity. 353 60

A 23-year-old male whose uncle died of nephronophthisis, and whose pathology is also discussed, presented with 5 g of protein in a 24-hour urine collection. Nephrogenic diabetes insipidus and salt wasting were present in addition to azotemia. Characterization of the proteinuria, including elevated alpha globulins by electrophoresis and markedly elevated urinary beta-microglobulins by radioimmunoassay (49.55 mg/L) indicated predominantly tubular proteinuria. A percutaneous renal biopsy showed normal glomeruli, interstitial inflammation and fibrosis, and tubular atrophy. Electron microscopy revealed notable alterations of the tubular basement membrane.
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PMID:Nephronophthisis with massive proteinuria. 618 93

Interstitial nephritis consequent to rifampin was associated with potassium wasting, an acidifying defect, high fractional uric acid excretion, and glucosuria, indicating a multiplicity of renal tubular transport abnormalities. Enlarged kidneys on sonogram and proteinuria were also observed.
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PMID:Potassium wasting and other renal tubular defects with rifampin nephrotoxicity. 651 18

X-linked recessive nephrolithiasis (XRN) was described in a large kindred in which nephrolithiasis; proximal tubular dysfunction, proteinuria, nephrocalcinosis, and renal failure occur only in males. Carrier females are asymptomatic, but formal studies of them have not been done. The gene for XRN has been mapped to the pericentromeric region of the X chromosome, close to the loci for several eye disease genes. We studied six affected males, 13 carrier females, and 25 normal members of this family including 7 females whose genetic haplotype predicted them to be carriers. Studies were done in the Clinical Research Unit on a diet containing 400 mg of calcium and 2 g of sodium, and by an additional outpatient urine collection was obtained on a 1-g calcium intake. Hypercalciuria occurred in five of six affected males, 4 of 12 carrier females, and three of seven predicted carriers. Significant proteinuria was present in all affected males and in no other subjects. Low-molecular-weight proteinuria was present in all affected males: the excretion of alpha 1-microglobulin exceeded normal by 3- to 14-fold, of beta 2-microglobulin exceeded normal by 100- to 400-fold, and of retinol-binding protein exceeded normal by 1,000- to 3,000-fold. The excretion of these proteins was less strikingly elevated in carrier females, but the excretion of alpha 1-microglobulin was abnormal in 9 of 15 carriers, beta 2-microglobulin was abnormal in 12 of 15, and retinolbinding protein in was abnormal 12 of 13, and this pattern was similar in predicted carriers. The urinary concentrating ability was abnormal in four affected males with renal insufficiency but normal in all other subjects. Urinary wasting of potassium, phosphorous, and glucose occurred infrequently, and no subject was hypouricemic. Formal ophthalmologic studies were normal in five affected males. Thus, the most consistent urinary abnormalities in XRN are hypercalciuria and low-molecular-weight proteinuria, the latter of which appears to be a marker for the carrier state.
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PMID:Characterization of carrier females and affected males with X-linked recessive nephrolithiasis. 770 83

Ifosfamide and cisplatin are two commonly used cancer chemotherapeutic agents associated with significant acute and chronic renal toxicity. The clinical characteristics of ifosfamide-induced renal injury are proximal tubular wasting of glucose, phosphate, bicarbonate, sodium, potassium, and amino acids; proteinuria; and decreased glomerular filtration rate. Cisplatin administration may result in a dose-dependent reduction of glomerular filtration rate, hypomagnesemia, hypokalemia, and polyuria. The characteristics of renal toxicity associated with each of these agents are discussed with attention to possible mechanisms of injury and long-term clinical outcome.
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PMID:Renal toxicity of cancer chemotherapeutic agents in children: ifosfamide and cisplatin. 778 38


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