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 six-month-old Labrador retriever was presented for investigation of acute polyuria, polydipsia and haematemesis six hours following ingestion of a tube of the topical antipsoriatic vitamin D analogue, calcipotriol. Transient hypercalcaemia, azotaemia, proteinuria, thrombocytopenia and ventricular arrhythmias ensued. Abdominal ultrasonography and echocardiography revealed evidence of diffuse soft tissue mineralisation. Despite 13 days of intensive supportive care, the dog was euthanased due to continued haematemesis and anorexia. Necropsy confirmed mineralisation and necrosis of multiple organ systems consistent with vitamin D toxicity.
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PMID:Calcipotriol toxicity in a dog. 1064 1

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 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

A four-month-old male Labrador retriever was presented for polyuria, polydipsia and persistent euglycaemic glucosuria. On referral, diagnostic tests demonstrated abnormal fractional excretions of electrolytes, increased urinary excretion of selected amino acids, mild renal tubular acidosis and mild proteinuria, indicating renal tubular dysfunction. Pyelonephritis was suspected and potentiated amoxycillin was administered. On re-evaluation at six months of age, the dog was no longer polyuric or polydipsic and the metabolic abnormalities associated with the tubulopathy had resolved. Transient Fanconi's syndrome has not previously been reported in small animals. This report demonstrates the potential for recovery of function in cases presenting with renal tubulopathies.
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PMID:Transient renal tubulopathy in a Labrador retriever. 1172 83

Ten patients of nephropathic cystinosis were admitted during the period 1995-2000. Their mean age was 12 months. The signs of failure to thrive and advanced rickets were seen in all patients. Other features included polyuria, polydipsia, pathologic fractures and deafness. Laboratory findings included glucosuria, hyposthenuria, hypocalcemia, proteinuria and azotemia. Therapy with phosphocysteamine showed marked clinical improvement.
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PMID:Infantile cystinosis. 1255 13

Four patients who had ingested large amounts of phenacetin-salicylate medications were studied during a 12-month period. Renal failure had progressed slowly over a number of years. All patients took the drug because of psychogenic headache. Considerable skill was required to elicit the history of drug habituation. The major features of the nephropathy were multiple episodes of metabolic acidosis, minimal proteinuria, pyuria but no bacteriuria, and polyuria and polydipsia early in the course of drug ingestion. Papillary necrosis was not a prominent clinical feature of this series. Discontinuation of drug ingestion by one patient was associated with recovery of a considerable degree of renal function. Preliminary experimental evidence obtained in the dog suggests that salicylate impaired the efficiency of the counter-current multiplier by decreasing sodium transport in the ascending limb of Henle, and decreased the permeability to water of the distal convoluted and collecting tubule; phenacetin had no such effect.
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PMID:PHENACETIN NEPHROPATHY. 1422 36

Tenofovir disopril fumarate, a new nucleotide analogue against human immunodeficiency virus-1 (HIV-1), can induce hypophosphataemia, the mechanism of which is unclear. Moreover, a renal tubulopathy can occur in long-term treated patients, as observed in 2 HIV-1-infected patients after 12 months of tenofovir therapy, with polyuria-polydipsia, proteinuria, glycosuria and amino-aciduria, which resolved after discontinuation of tenofovir. The risk of renal tubulopathy symptoms in patients on long-term tenofovir therapy should be noted.
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PMID:Tubulopathy consecutive to tenofovir-containing antiretroviral therapy in two patients infected with human immunodeficiency virus-1. 1530 94

This study was conducted with 3 objectives in mind: first, to identify the toxic fraction (aqueous or organic) in leaves and flowers; second, to identify diagnostic marker(s) of toxicosis in cats; and, third, to evaluate the morphologic effects of intoxication. The study was conducted in 2 phases. Phase 1 was to identify which extract, organic or aqueous, was nephrotoxic and also to determine the appropriate dose for use in the phase 2 studies. Results indicated that only the aqueous extracts of leaves and flowers were nephrotoxic and pancreotoxic. To identify the proximate toxic compound, cats in the phase 2 study were orally exposed to subfractions of the aqueous flower extract, 1 subfraction per cat. Results confirmed vomiting, depression, polyuria, polydipsia, azotemia, glucosuria, proteinuria, and isosthenuria as toxic effects of the Easter lily plant. Another significant finding in serum was elevated creatinine kinase. Significant histologic kidney changes included acute necrosis of proximal convoluted tubules and degeneration of pancreatic acinar cells. Renal ultrastructural changes included swollen mitochondria, megamitochondria, edema, and lipidosis. Subfraction IIa3 of the aqueous floral extract contained most of the toxic compound(s). These studies reproduced the clinical disease, identified the most toxic fraction of the Easter lily, and helped characterize the clinical pathology, histopathology, and ultrastructural pathology associated with the disease.
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PMID:A comprehensive study of Easter lily poisoning in cats. 1558 68

Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.
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PMID:A case of insulin edema with inappropriate hyperaldosteronism. 1576 45


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