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 reduction of renal kallikrein has been found in non-insulin-treated diabetic individuals, suggesting that an impaired renal kallikrein-kinin system (KKS) contributes to the development of diabetic nephropathy. We analyzed relevant components of the renal KKS in non-insulin-treated streptozotocin (STZ)-induced diabetic rats. Twelve weeks after a single injection of STZ, rats were normotensive and displayed hyperglycemia, polyuria, proteinuria, and reduced glomerular filtration rate. Blood bradykinin (BK) levels and prekallikrein activity were significantly increased compared with controls. Renal kallikrein activity was reduced by 70%, whereas urinary BK levels were increased up to threefold. Renal kininases were decreased as indicated by a 3-fold reduction in renal angiotensin-converting enzyme activity and a 1.8-fold reduction in renal expression of neutral endopeptidase 24.11. Renal cortical expression of kininogen and B2 receptors was enhanced to 1.4 and 1. 8-fold, respectively. Our data suggest that increased urinary BK levels found in severely hyperglycemic STZ-diabetic rats are related to increased filtration of components of the plasma KKS and/or renal kininogen synthesis in combination with decreased renal kinin-degrading activity. Thus, despite reduced renal kallikrein synthesis, renal KKS is activated in the advanced stage of diabetic nephropathy.
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PMID:Functional, biochemical, and molecular investigations of renal kallikrein-kinin system in diabetic rats. 1060 Aug 53

Membranoproliferative glomerulonephropathy was diagnosed in 5 of 7 adult Beagles from the same litter. Dogs were raised in more than 1 area of the United States. One died without evidence of renal disease when it was 3 years old. At 8 years of age, 2 dogs developed signs of uremia, including polyuria, polydipsia, and infrequent episodes of anorexia and vomiting. Serum biochemical variables and urine specific gravity values were consistent with renal azotemia. Both dogs had proteinuria. Although healthy, 3 of the 4 remaining Beagles had proteinuria. Of these 3, only 1 was azotemic. Membranoproliferative glomerulonephritis was diagnosed on the basis of results of histologic examination of renal biopsy specimens from 4 of the dogs. Electron microscopy performed on 3 of the renal biopsy specimens revealed identical lesions, consisting of an extremely thickened glomerular basement membrane with multilaminar splitting. Immunoglobulin or amyloid deposits were not detected. On the basis of similar clinicopathologic abnormalities, common genetic background, and identical histopathologic and electron microscopic findings, familial renal disease was diagnosed. Additional studies involving other related Beagles are needed to identify the hereditary nature of membranoproliferative glomerulonephropathy in Beagles.
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PMID:Familial glomerulonephropathy in a litter of beagles. 1063 17

India is amidst a demographic transition showing an ageing trend. This will increase non-communicable diseases including diabetes which is already showing an increasing trend. With scanty literature existing on elderly diabetics (> 60 years of age), it was decided to study the clinico-laboratory and complication profile of this group of patients. Fifty consecutive elderly diabetics were studied and evaluated for ECG, chest x-ray, blood sugar, urea, creatinine, lipid profile, proteinuria, motor nerve conduction velocity and autonomic neuropathy. Duration of diabetes varied from one month to 28 years. Fifty-six per cent of the patients presented with classical symptoms of polyuria, polyphagia and polydipsia. Hypertension was present in 40% and cataract in 54% of the patients. Eighteen per cent were obese, 52% had evidence of peripheral neuropathy while 56% had autonomic neuropathy. Background diabetic retinopathy was present in 56%, pre-proliferative retinopathy and maculopathy in 4% each; hypertensive retinopathy in 10% of patients; 44% had microproteinuria and 8% had chronic renal failure. Hypercholesterolaemia was present in 64% and hypertriglyceridaemia in 42% of the patients with 26% having coronary artery disease. Sixty per cent were harbouring infections--20% had foot infections, 14% had tuberculosis and 10% had urinary tract infections. Ninety-two per cent of the patients were aware of their disease but 62% were not aware of the complications and of the need for strict dietary and drug compliance. There was a high prevalence of associated diseases viz, osteoarthritis, cataract, hypertension, hepatitis and parkinsonism. Therefore, this study brings out the need to have a holistic and multidisciplinary approach for management of elderly diabetics who constitute a heterogeneous group with distinct health care problems.
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PMID:Clinical and laboratory profile of diabetes in elderly. 1065 95

We have used homologous recombination to disrupt the mouse gene coding for the NaK2Cl cotransporter (NKCC2) expressed in kidney epithelial cells of the thick ascending limb and macula densa. This gene is one of several that when mutated causes Bartter's syndrome in humans, a syndrome characterized by severe polyuria and electrolyte imbalance. Homozygous NKCC2-/- pups were born in expected numbers and appeared normal. However, by day 1 they showed signs of extracellular volume depletion (hematocrit 51%; wild type 37%). They subsequently failed to thrive. By day 7, they were small and markedly dehydrated and exhibited renal insufficiency, high plasma potassium, metabolic acidosis, hydronephrosis of varying severity, and high plasma renin concentrations. None survived to weaning. Treatment of -/- pups with indomethacin from day 1 prevented growth retardation and 10% treated for 3 weeks survived, although as adults they exhibited severe polyuria (10 ml/day), extreme hydronephrosis, low plasma potassium, high blood pH, hypercalciuria, and proteinuria. Wild-type mice treated with furosemide, an inhibitor of NaK2Cl cotransporters, have a phenotype similar to the indomethacin-rescued -/- adults except that hydronephrosis was mild. The polyuria, hypercalciuria, and proteinuria of the -/- adults and furosemide-treated wild-type mice were unresponsive to inhibitors of the renin angiotensin system, vasopressin, and further indomethacin. Thus absence of NKCC2 in the mouse causes polyuria that is not compensated elsewhere in the nephron. The NKCC2 mutant animals should be valuable for uncovering new pathophysiologic and therapeutic aspects of genetic disturbances in water and electrolyte recovery by the kidney.
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PMID:Uncompensated polyuria in a mouse model of Bartter's syndrome. 1077 55

We report a woman with a history of allergies, polyuria, polydipsia, proteinuria, renal loss of electrolytes, renal tubular acidosis, nephrocalcinosis, and palpable purpura. A proximal defect was excluded by a normal bicarbonate reabsorption curve, and a distal tubular defect was shown because urine pH did not decrease to less than 6.4 despite ammonium chloride-induced systemic acidosis. Moreover, furosemide failed to improve urinary acidification. Urine-to-blood PCO(2) gradient was less than 14 mm Hg, although the urine bicarbonate level reached values as high as 89 mEq/L. Combining bicarbonate and neutral phosphate infusions increased the urine-to-blood PCO(2) gradient to only 20 mm Hg. These subnormal PCO(2) gradient values point to proton-pump dysfunction in the collecting tubule. Histological evidence of tubulointerstitial disease accompanied the tubular defects. The striking histological feature was the presence of immunoglobulin E (IgE) deposits in glomeruli, tubuli, and vessels. Concurrent with these findings, she had high serum IgE titers and CD23 levels. IgE antibodies from her serum were reactive against human renal tubuli, with binding to two regions that matched two different proteins present in cortex and medulla. One of these proteins corresponded to carbonic anhydrase II (31 kd); the second, to an unidentified protein that seems attached to cell membranes. We suggest that these IgE antibodies could have had a pathogenic role in this patient's glomerular, tubular, and small-vessel disease.
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PMID:Renal tubular acidosis and vasculitis associated with IgE deposits in the kidney and small vessels. 1079 31

Acute tubulo-interstitial nephritis and uveitis (TINU syndrome) in a 53-year-old woman is reported. This rare syndrome was described 27 years ago by Dobrin et al. Since then about 50 cases have been described. The syndrome can appear at any age but most patients are under 20 years; about 75% are females. Clinical characteristics include fatigue, general malaise, weight loss, fever, night sweats, anorexia, nausea and vomiting, pallor, nocturia, polyuria, arthralgia and skin rash. Ocular involvement usually includes anterior uveitis but is sometimes posterior; in most cases the uveitis is bilateral. The characteristic laboratory findings are anemia, rapid sedimentation rate, decreased glomerular filtration rate with increased serum creatinine and urea. Total protein is increased because of polyclonal gammopathy and elevated beta 2-microglobulin. Urinalysis characteristically reveals proteinuria and beta 2-microglobulinuria. The histopathologic features on renal biopsy are characteristic of tubulo-interstitial nephritis. Uveitis can precede, accompany or follow onset of the nephropathy. The pathogenesis and etiology of the syndrome are as yet unknown. Treatment consists of large doses of corticosteroids, but the necessity for treatment is unclear, since there is evidence of spontaneous improvement. Although the prognosis of the nephropathy is favorable and most cases are reversible, the uveitis tends to recur.
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PMID:[Tubulo-interstitial nephritis and uveitis syndrome--TINU syndrome]. 1088 33

ABSTRACT.: Tissue content of advanced glycation end products (AGE) increases with age and contributes to the changes in structure and function of the renal and cardiovascular systems. The effect of chronic food restriction on this AGE accumulation was investigated in lean WAG/Rij rats. A 30% food restriction performed from 10 to 30 mo in female rats reduced their mean body weight from 240 +/- 7 to 160 +/- 12 g, but did not modify their survival. AGE collagen content increased from 14.3 +/- 5.5 to 104.7 +/- 13.0 arbitrary units per microgram (AU/microg) of hydroxyproline (OHPro) in kidney between 10 and 30 mo, and from 9.7 +/- 1.2 to 310.6 +/- 34.6 AU/microg OHPro in the abdominal aorta. Food restriction reduced AGE accumulation to 21.4 +/- 3.3 and 74.6 +/- 16.5 AU/microg OHPro in kidney and aorta of 30-mo-old animals. Similar results were found for collagen prepared from isolated glomeruli (7.8 +/- 1.2, 81.2 +/- 16.1, and 10.3 +/- 4.3 AU/microg OHPro in 10-mo, 30-mo, and restricted 30-mo-old rats). Reduction of intrarenal and arterial AGE accumulation by food restriction was confirmed by immunostaining in optical microscopy. Age-related changes in arterial and kidney structures as polyuria and proteinuria were mainly prevented by food restriction. These data indicate that chronic food restriction reduces the accumulation of AGE and preserves the structure and function of the renal and cardiovascular systems in learn rats, although it did not affect survival of the animals between 10 and 30 mo.
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PMID:Food restriction prevents advanced glycation end product accumulation and retards kidney aging in lean rats. 1090 62

Because cystinotic patients are polyuric and may have severe proteinuria, each of which is a potential risk factor for graft thrombosis, preemptive transplantation for them is questionable. The objectives of this study were to characterize the changes in urine volume and protein excretion at various stages of cystinosis, determine whether there is serologic evidence of hypercoagulability, and review the clinical experience in renal transplantation in cystinotic children. The records of cystinotic patients followed at the Montreal Children's Hospital between 1992 and 1998 were reviewed. Urinary volume, protein excretion, and coagulation markers were collected to determine the glomerular filtration rate (GFR) >50 ml/min/1.73 m2, <20 ml/min/1.73 m2, before and after starting dialysis. In addition, graft failure and graft thrombosis rates were obtained from the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) database. Urinary volume and protein excretion remained elevated throughout different phases of the disease. Coagulation factors were within normal limits for all patients. In the NAPRTCS database there were four thromboses among the 114 patients transplanted cystinotic patients. All these occurred in cadaveric grafts and only one occurred after preemptive transplantation. Despite polyuria and severe proteinuria, children with cystinosis do not appear to be at an increased risk of graft failure or graft thrombosis.
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PMID:Polyuria and proteinuria in cystinosis have no impact on renal transplantation. A report of the North American Pediatric Renal Transplant Cooperative Study. 1109 1

Nephrotoxicity is an inherent adverse effect of certain anticancer drugs. Renal dysfunction can be categorised as prerenal uraemia, intrinsic damage or postrenal uraemia according to the underlying pathophysiological process. Renal hypoperfusion promulgates prerenal uraemia. Intrinsic renal damage results from prolonged hypoperfusion, exposure to exogenous or endogenous nephrotoxins, renotubular precipitation of xenobiotics or endogenous compounds, renovascular obstruction, glomerular disease, renal microvascular damage or disease, and tubulointerstitial damage or disease. Postrenal uraemia is a consequence of clinically significant urinary tract obstruction. Clinical signs of nephrotoxicity and methods used to assess renal function are discussed. Mechanisms of chemotherapy-induced renal dysfunction generally include damage to vasculature or structures of the kidneys, haemolytic uraemic syndrome and prerenal perfusion deficits. Patients with cancer are frequently at risk of renal impairment secondary to disease-related and iatrogenic causes. This article reviews the incidence, presentation, prevention and management of anticancer drug-induced renal dysfunction. Dose-related nephrotoxicity subsequent to administration of certain chloroethylnitrosourea compounds (carmustine, semustine and streptozocin) is commonly heralded by increased serum creatinine levels, uraemia and proteinuria. Additional signs of streptozocin-induced nephrotoxicity include hypophosphataemia, hypokalaemia, hypouricaemia, renal tubular acidosis, glucosuria, aceturia and aminoaciduria. Cisplatin and carboplatin cause dose-related renal dysfunction. In addition to increased serum creatinine levels and uraemia, electrolyte abnormalities, such as hypomagnesaemia and hypokalaemia, are commonly reported adverse effects. Rarely, cisplatin has been implicated as the underlying cause of haemolytic uraemic syndrome. Pharmaceutical antidotes to cisplatin-induced nephrotoxicity include amifostine, sodium thiosulfate and diethyldithiocarbamate. Dose- and age-related proximal tubular damage is an adverse effect of ifosfamide. In addition to renal wasting of electrolytes, glucose and amino acids, Fanconi syndrome, rickets and osteomalacia have occurred with ifosfamide treatment. High dose azacitidine causes renal dysfunction manifested by tubular acidosis, polyuria and increased urinary excretion of electrolytes, glucose and amino acids. Haemolytic uraemia is a rare adverse effect of gemcitabine. Methotrexate can cause increased serum creatinine levels, uraemia and haematuria. Acute renal failure is reported following administration of high dose methotrexate. Urinary alkalisation and hydration confer protection against methotrexate-induced renal dysfunction. Dose-related nephrotoxicity, including acute renal failure, are reported subsequent to treatment with pentostatin and diaziquone. Acute renal failure is a rare adverse effect of treatment with interferon-alpha. Haemolytic uraemic syndrome occurs with mitomycin administration. A mortality rate of 50 to 100% is reported in patients developing mitomycin-induced haemolytic uraemic syndrome. Capillary leak syndrome occurring with aldesleukin therapy can cause renal dysfunction. Infusion-related hypotension during infusion of high dose carmustine can precipitate renal dysfunction.
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PMID:Anticancer drug-induced kidney disorders. 1121 85

Autosomal dominant familial nephropathies with adult onset, no macroscopic cysts, and progressive deterioration include medullary cystic disease (ADMCKD) as well as other less specific entities. We studied a kindred of Jewish ancestry in which 15 members (both male and female) have suffered from chronic renal failure. The first evidence of renal involvement was observed between 18 and 38 years. It included hypertension followed by progressive renal insufficiency. No polyuria, anemia, gout, hematuria, nor proteinuria were seen. An average of 4.5 years elapsed from diagnosis to end-stage renal disease. Renal pathology at early stages of the disease showed extensive tubulointerstitial fibrosis and global glomerulosclerosis. Linkage analysis was performed at the two known loci of ADMCKD, on Chromosomes 1 and 16. Linkage to the chromosome 16 locus was excluded. However, linkage to the chromosome 1q21 locus of ADMCKD was established with a maximum two-point LOD score of 3.82 to D1S394. The disease interval could be narrowed to about 9 cM/7.4 Mb between D1S1156 and D1S2635. Multiple-point linkage analysis revealed a maximum LOD of 4.21, with a broad peak from markers D1S2858 and D1S2624. This report establishes linkage between a familial nephropathy characterized by hypertension and progressive renal failure to the locus described for ADMCKD, a disease classically associated with macroscopic corticomedullary cysts, salt-losing tubulointerstitial nephropathy, and anemia. This finding broadens the clinical spectrum of ADMCKD positioned on chromosome 1q21 locus.
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PMID:Clinical and genetic characterization of an autosomal dominant nephropathy. 1124 91


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