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)

The clinical and necropsy findings on 7 patients with monoclonal immunoglobulin light chain deposition nephropathy are described (4 cases with a myelomatous and 3 with a non-myelomatous background). All patients had moderate proteinuria and progressive azotemia. Three myelomatous and all three non-myelomatous patients died from uremia after a mean time of 12 and 23 months, respectively, from the first presentation. Immunohistochemically, 6 patients had kappa, and one had lambda light chain deposition. Light microscopically, interstitial fibrosis, tubular atrophy and arteriolar hyalinosis were present in all cases. The glomeruli showed no changes (1 case), or displayed patterns of mesangial widening: mild (1 case), nodular (mesangial nodules, 4 cases) or global lobular expansion (1 case). Mesangial nodules were observed either with or without lamellation. Around the nodules, microaneurysms were seen in 2 cases. Mesangial nodular expansion was accompanied by crescents in 56% of the glomeruli in a male patient suffering from kappa light chain deposition nephropathy without myeloma. The present findings and a review of the literature indicate the following mesangial changes in light chain deposition nephropathy: 1. no changes, 2. mild expansion, 3. nodular expansion with and without lamellation, and 4. lobular expansion. Subtypes 2, 3 and 4 may be present in parallel, may occur with or without cellular proliferation, and may be accompanied by crescents. The term nodular glomerulosclerosis to describe mesangial nodular expansion is not completely correct, and hence its use is not recommended.
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PMID:Light chain deposition nephropathy in necropsy material. 176 89

Rats made uremic by 2-stage 5/6 nephrectomy and sham-operated control animals were fed either a normal laboratory chow, a high-sucrose (60%) or a high-fat (10% cholesterol; 20% olive oil) diet, all containing 21% protein and identical amounts of electrolytes, vitamins and trace elements. Serum creatinine levels remained unchanged in the control animals but rose in the 5/6 nephrectomised uremic animals by a factor of 2.7 from a mean of 0.44 +/- 0.05 mg/dl to 1.20 +/- 0.11 mg/dl at 8 weeks, without differences between the dietary groups. During 8 weeks of dietary regimen the high-sucrose and high-fat diets induced significant hypertriglyceridemia, generally similar in control and uremic rats. The uremic animals on a high-sucrose and high-fat diet had the most pronounced rise in serum triglycerides, 331.5 +/- 89.0 and 298.0 +/- 45.0 mg/dl, respectively (control: 159.9 +/- 14.0 mg/dl). After 4 and 8 weeks, only the animals on the high-fat diet had significant hypercholesterolemia, most pronounced in the uremic animals (356 +/- 56.3 mg/dl; control: 71.6 +/- 12.9 mg/dl). The animals in the latter group also had significant proteinuria and renal histologic abnormalities consisting of xanthoma-like glomerular lesions, infiltrates and fibrosis not seen in the other groups of animals. These data indicate that dietary-induced hyperlipidemia of short duration causes or aggravates renal damage in the rat with mild-moderate uremia, induced by ablation.
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PMID:Dietary-induced hyperlipidemia and renal function in the uremic rat. 186 74

23 patients (16 women, 7 men) with rheumatoid arthritis (RA) and renal biopsy-proven mesangial glomerulopathy (MGP) were followed for 4-117 months (median 42) in order to evaluate the clinical course of their renal disease. Urinalysis was made, and 24-hour urine protein excretion and serum creatinine were determined. At the time of renal biopsy, the clinical renal findings of the patients were isolated hematuria (n = 10), isolated proteinuria (n = 6) and hematuria combined with proteinuria (n = 7). Hematuria persisted and renal function remained normal in all patients with isolated hematuria. A possible association between the presence of hematuria and the use of antirheumatic drugs was not established in this study. Proteinuria was clinically closely associated with the use of antirheumatic drugs in 9 out of 13 cases (6 with gold sodium thiomalate, 2 with D-penicillamine and 1 with auranofin) suggesting that antirheumatic drugs are important contributors to proteinuria in these patients. Renal function, although initially reduced in some patients, remained stable in all but 1 patient with IgA glomerulonephritis who developed the nephrotic syndrome and died of uremia. In conclusion, the clinical course of MGP in RA patients is benign in most patients. Moreover, this nephropathy may not represent a clinical entity. Proteinuria was related to antirheumatic drugs in most patients whereas microhematuria was constant even after stopping the antirheumatic drugs.
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PMID:Mesangial glomerulopathy in rheumatoid arthritis patients. Clinical follow-up and relation to antirheumatic therapy. 194 47

In the patient with diabetes mellitus the onset of intermittent and then persistent proteinuria signals the development of established nephropathy. This heralds an extremely poor prognosis and mortality in this group has been estimated to be 80 to 100 times greater than that of an age-matched normal population. The excess mortality and its associated morbidity exists for both insulin-dependent and non-insulin-dependent patients who develop proteinuria. The final cause of death is often cardiovascular, such as myocardial infarction or a cerebrovascular accident, rather than end stage renal failure with death from uraemia. Strict and aggressive control of blood pressure during this stage is the only therapy that has been shown to slow the decline in glomerular filtration. To date, there have been no studies large enough to establish if this can produce the desired effect of reducing the excess mortality in this group. The newer antihypertensive agents may have a specific role but this also remains to be shown conclusively; their major advantage may be related to their fewer side-effects especially on cardiovascular risk factors in this highly susceptible group.
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PMID:Hypertension and prognosis in established diabetic nephropathy. 195 24

A 59-year-old man with a 10-year history of hypertension was admitted to the Osaka Medical College Hospital because of left shoulder pain, lower blood pressure in left arm, and nasal lower quadrant defect of the visual field of the left eye. After admission, he underwent coronary angiography and aortography. The examinations revealed that, although coronary arteries were normal, the orifice of the left subclavian artery was occluded almost completely. Two weeks after the examination, he underwent intra arterial DSA of the cerebral artery. After manipulation of the DSA, the patient complained of severe calf pain, developed blue toe and progressive renal failure with severe proteinuria. He died of uremia about three months after the DSA. Autopsy revealed multiple cholesterol emboli in small arteries in the visceral organs, urogenital organs and thyroid gland. In the kidneys, especially, damage by cholesterol emboli was large with irregular cortical necrosis. Examination of the brain was not permitted. This case shows that cholesterol embolism of the kidneys can be a lethal complication of angiography.
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PMID:[An autopsy case of renal failure due to cholesterol embolism following angiography]. 201 3

Similarities between atherosclerosis and glomerulosclerosis suggest that hyperlipidaemia may contribute to glomerular injury. Dietary supplementation with 4% cholesterol + 1% cholic acid was administered to rats 4 weeks after 1 1/3 nephrectomy and continued for 7 weeks. There was a significant increase in serum cholesterol (peak = 11.52 +/- 1.09 mmol l-1 vs. 4.73 +/- 0.31 on control diet, P less than 0.001) and triglyceride concentrations (peak = 2.31 +/- 0.27 mmol l-1 vs. 1.41 +/- 0.29, P less than 0.05) and a marked increase in beta-migrating lipoproteins. The severity of hypercholesterolaemia was significantly correlated with proteinuria (control diet: r = 0.600, cholesterol diet: r = 0.672, P less than 0.0001) as was hypertriglyceridaemia (control diet: r = 0.544, cholesterol diet: r = 0.678, P less than 0.0001). The percentage of glomeruli containing lipid deposits was increased from 21% to 60% (P less than 0.05). The kidney total cholesterol content was increased from 29.2 +/- 0.8 to 47.7 +/- 3.3 mumols g-1 dry weight (P less than 0.0001), with esterified cholesterol increasing from 7.5 +/- 0.4% to 14.5 +/- 2.1% of total (P less than 0.01). Serum cholesterol concentration was significantly correlated with both glomerular lipid deposition (rs = 0.7195, P less than 0.0001) and tissue total cholesterol content (rs = 0.6053, P less than 0.001). Lipid vacuolation was prominent in the paramesangium and within mesangial cells. Despite these changes hypertension, uraemia, proteinuria and glomerulosclerosis were not significantly increased on the cholesterol diet. Cholesterol deposition in the glomeruli occurs secondary to hyperlipidaemia in rats following subtotal nephrectomy but over 7 weeks no exacerbation of glomerulosclerosis is detectable.
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PMID:The role of lipids in the pathogenesis of glomerulosclerosis in the rat following subtotal nephrectomy. 210 41

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest hereditary nephropathy. We collected 92 cases in VGH. Diagnosis was confirmed by intravenous pyelogram, renal sonogram, or renal CAT scan. The incidence of having positive family history was just only 28.3%. Patients were diagnosed at the mean age of 54 +/- 11 years (26-74 years). The common clinical findings were hypertension (73.9%), abdominal mass, proteinuria, anemia, azotemia, abdominal or back pain and pyuria in orders. Hypertension might present in the early stage with normal renal function (near 40%). Polycystic liver was the major extrarenal lesion (57.6%), but the incidence of abnormal liver function was only 10.1%. Enlarged kidneys were not always palpable, even at end stage of renal function (mean age 56 +/- 9 years, 89.4% kidney palpable). Patient's urine amount was usually nonoliguric, even in uremic stage (82.9%). Sepsis was the first cause of death. Cardiovascular disease and uremia were followed in sequence. Their expired mean age was 61 +/- 7 years (53-74 years).
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PMID:[Autosomal dominant polycystic kidney disease clinical analysis in VGH--Taipei]. 217 45

Diabetic nephropathy is now the leading cause of renal failure in patients referred for uremia therapy. The diabetic patient is a complicated treatment problem from the first detection of microalbuminmuria, at which time decisions regarding choice of antihypertensive and strictness of metabolic control assume increasing importance. At present, our policy is to advocate strict control of blood pressure, aiming for a systolic blood pressure of less than 140 mm Hg and a diastolic blood pressure of less than 80 mm Hg. We attempt to maintain hemoglobin Alc levels at less than 8%, if the patient does not develop frequent episodes of hypoglycemia. We extend these recommendations to the patient with frank proteinuria, nephrotic syndrome and early uremia, understanding that strict metabolic control may be impossible as patients lose GFR. In addition, we recommend avoidance of a high protein diet in the early nephropathic diabetic, with diet of approximately 1 gm/kg/d. As renal failure progresses, we embark on an analysis of the patient's abilities, lifestyle, and social support. At a GFR of approximately 10 mL/min, we initiate preparations for uremia therapy. If a willing and appropriate living related kidney donor is available, the patient is referred for cardiovascular evaluation and kidney transplantation performed subsequently. If no donor is immediately available, we refer the patient for vascular access placement and/or insertion of a Tenckhoff peritoneal catheter, if preferred. Most of these predialysis patients also undergo screening for placement on the cadaveric kidney transplant list, including cardiac work-up as is done for the patients who receive living-related renal transplants. Because of the long waiting list in Brooklyn, and the universal shortage of organ donors, many of these patients eventually end up on dialysis for some period of time. Other extrarenal problems (urologic, ophthalmologic) are addressed at initial referral and followed up, in hopes of maintaining the patient in optimal physical shape as uremia progresses. The care of the diabetic patient with ESRD ideally involves a consortium of caregivers. We include a nurse-educator familiar with options for uremia therapy, a podiatrist, a cardiologist, and often a urologist, an endocrinologist, and a gastroenterologist. In addition, a social worker is helpful to assess psychologic difficulties in adjustment to uremia, socioeconomic considerations, and rehabilitation status. Finally, the nephrologist, as coordinator of this team works with the vascular or transplant surgeon, to facilitate the transition to ESRD and its therapy.
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PMID:Care of the diabetic patient with end-stage renal disease. 219 Feb 84

Experimental and spontaneous infections with Corynebacterium suis in sows were investigated. In early stages animals show no clinical disorders or only for a short time. However, there are already marked changes in urinary samples (hematuria, proteinuria, leukocyturia, gross alterations). Using an endoscope mucosal irritations can be seen mainly on the floor of the bladders. In chronic cases alterations in urine are more pronounced. If a pyelonephritis is present in addition to the cystitis, general signs of illness are evident including anorexia, emaciation, anemia, subnormal body temperature and abortions. Bladders demonstrate an erosive and ulcerative, hemorrhagic cystitis on the whole mucosal surface. Uremia appears only in late stages of the disease.
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PMID:[Corynebacterium suis infection in swine. 1. Clinical diagnosis with special consideration of urine studies and cystoscopy]. 221 5

Twenty-two patients with definite or classical rheumatoid arthritis (RA) who were diagnosed as amyloidosis by biopsy or at autopsy were investigated. The average duration of RA prior to the diagnosis of amyloidosis was 16.5 +/- 12.5 years. The symptoms that led to the diagnosis of amyloidosis were renal symptoms in 11 cases and gastrointestinal symptoms in 5 cases. Urinary protein was positive in 16 cases (73%). The degree of proteinuria varied in each case. Nephrotic syndrome was observed in 5 cases. Azotemia (Cr greater than 1.5 mg/dl) was present in 18 cases (82%). The period from the diagnosis of amyloidosis to death was 3.0 +/- 2.2 years. The causes of death were uremia in 10 cases, heart failure in 2 cases, malignancy in 2 cases, sepsis in 2 cases and others in 2 cases. Thirteen patients were autopsied and the frequency of amyloidosis complicated with RA was 22.0% in autopsied rheumatoid patients. Although nephropathy was present in most cases of amyloidosis complicated with RA, proteinuria and azotemia greatly varied in both degree and course.
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PMID:Clinical studies on amyloidosis complicated with rheumatoid arthritis--with particular reference to nephropathy. 227 6


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