Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Outpatient hyperkalemia" is a new clinical syndrome in which high serum potassium levels (SK) are found in the outpatient condition returning toward normal without any specific treatment after admission to the hospital. We report here of six patients with high blood pressure of various origin (chronic glomerulonephritis, interstitial nephritis, diabetic nephropathy, Gordon syndrome) in whom dietary and postural factors were found to be responsible for the outpatient hyperkalemia. The Na content of the "ad libitum" outpatient diet was definitely higher than that of the regular hospital diet. Increasing the Na intake from 120 mEq to 300 mEq induced a marked elevation of SK (from 5.21 +/- 0.16 to 6.34 +/- 0.40 mEq/l; p less than 0.001) in two hospitalized, recombent patients. On the other hand, Na restriction induced a dramatic improvement in hyperkalemia (from 5.89 +/- 0.11 mEq/l to 4.79 +/- 0.08 mEq/l:; p less than 0.001) in 4 patients in whom the effect was studied in the outpatient state. Although the mean plasma aldosterone (PA) was significantly lower in the patient group than in the healthy group, during normal Na intake there was a considerable overlap. A clearer distintion was made by using the new index of PA per SK ratio expressing the diminution in the apparently normal PA when related to the abnormally high SK. During high Na intake, PA was definitely suppressed and during Na restriction there was a dramatic relief from suppression. The present studies confirmed the previously described phenomenon of "upright hyperkalemia" which may have played an additional role in the development of outpatient elevation of SK. The knowledge of the clinical syndrome of "outpatient hyperkalemia" may be important to single out certain cases of easily correctable insufficient (suppressed) aldosterone production.
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PMID:"Outpatient hyperkalemia" syndrome in renal and hypertensive patients with suppressed aldosterone production. 28 14

Dipeptidyl peptidase IV (EC 3.4.14.5) and angiotensinase A (EC 4.4.11.7) were purified to homogeneity from pooled urine concentrate of patients with renal damage, using ultrafiltration, ammonium sulphate precipitation, lectin affinity chromatography, FPLC-ion-exchange(Mono-Q-)chromatography, and FPLC-gel filtration (Superdex). Based on the specific enzyme activity of the starting material, dipeptidyl peptidase IV was enriched 1629 fold, angiotensinase A 1183 fold. The relative molecular masses, Michaelis constants and isoelectric points were determined. Negative staining of the purified enzymes revealed globular proteins (5-7 nm). Antisera raised against dipeptidyl peptidase IV and angiotensinase A reacted specifically with tubular and, in the case of anti-angiotensinase A sera, with tubular and glomerular structures. In addition, urinary membrane vesicles of proximal tubule origin were eluted with the void volume (Superdex-gel filtration), indicating heavy epithelial cell disintegration. Both soluble tissue enzymes (dipeptidyl peptidase IV, angiotensinase A) and vacuolar blebs shed from epithelia contribute to proteinuria, as was shown in patients with glomerulonephritis, interstitial nephritis, diabetic nephropathy and, for angiotensinase A, in patients with essential arterial hypertension.
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PMID:Biochemical and immunological properties of urinary angiotensinase A and dipeptidylaminopeptidase IV. Their use as markers in patients with renal cell injury. 136 94

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

We have conducted an immunocytochemical analysis to investigate the presence of the recently described vascular cell adhesion molecule-1 (VCAM-1) in human kidney, using the anti-VCAM-1 monoclonal antibody 1.4C3. In normal control tissue VCAM-1 was present on some (but not all) parietal epithelial cells lining Bowman's capsule. Forty-nine of fifty clinical biopsy specimens were characterised by the additional presence of VCAM-1 on proximal tubular cells. This was most marked in biopsies of patients with interstitial nephritis or systemic vasculitis with crescentic nephritis, but was also observed in biopsies with minimal change, IgA or lupus nephropathy, or from patients with diabetic nephropathy, amyloid, or gout. Proximal tubule VCAM-1 correlated significantly with the number of transferrin-receptor-positive leukocytes (r = 0.607, p less than 0.0001) in the interstitium, but not with expression of HLA-DR by tubular cells. Surprisingly, VCAM-1 was not observed on vascular endothelial cells in these biopsies, even in the presence of a marked infiltrate; this contrasts with other tissues (e.g. skin and synovium). The presence of VCAM-1 on tubular cells in the inflamed kidney indicates the potential for these cells to interact with mononuclear cells, either as accessory cells or as cytotoxic targets. The unexpected absence of VCAM-1 in renal vascular endothelial cells suggests local differences in the endothelial cells of this organ.
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PMID:Expression of VCAM-1 in the normal and diseased kidney. 172 89

A national sample of dialysis physicians was used to obtain data for a comparison of patient characteristics, comorbid conditions and treatment patterns associated with the five leading causes of end-stage renal disease (ESRD). The data are used to assess trends in physician care for ESRD patients and likely changes in program costs. The analysis shows that patients with glomerulonephritis are the youngest. Those with hypertensive nephropathy are the oldest, and include the highest proportion of blacks, while those with polycystic kidney disease include the lowest proportion of blacks. Patients with diabetic nephropathy have the most problems noted at the time of physician contact, the most emergent and severe problems, the highest number of diagnostic tests utilized, the most complex treatments required and the longest physician time spent per encounter. Patients with 'other interstitial nephritis' are significantly more likely to have infections, musculoskeletal disorders, chronic obstructive pulmonary disease and neoplasms noted as comorbid conditions. They also have the highest number of therapeutic procedures and the greatest percentage of referrals for consultations. Survey data highlight the evolving nature of Medicare's ESRD program. With increasing numbers of elderly and diabetic patients, more physician time will be required for the overall care of the dialysis patient, and increasing costs associated with necessary diagnostic tests and referrals can be expected.
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PMID:Dialysis for chronic renal failure: comorbidity and treatment differences by disease etiology. 266 70

The charts of 70 successive patients presenting for dialysis therapy for end-stage renal disease (ESRD) were evaluated for their serum electrolyte values. The "classical" pattern of low total CO2 (tCO2), elevated anion gap ("delta"), and normal chloride was found in a minority of patients (14 of 70, or 20%). Hyperchloremia was noted in 46%; in 21 patients (30%), this was associated with a normal delta and in 11 (16%), hyperchloremia was accompanied by an elevated delta. Fourteen patients (20%), most with diabetic nephropathy, had normal serum electrolytes. Patients with chronic glomerulonephritis had a hyperchloremic pattern as often as not, and two of four patients with interstitial nephritis demonstrated hyperchloremia without an elevated delta. We conclude that the previously held thesis that hyperchloremia is a rare or absent finding by the time renal failure progresses to ESRD is no longer tenable. Furthermore, a significant minority of ESRD patients may require the initiation of dialysis at a time when their serum electrolytes are still normal.
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PMID:Serum electrolyte patterns in end-stage renal disease. 309 Aug 75

9 consecutive cases of Legionnaires' disease are presented, all of which involved either a pathological urinary sediment or acute renal insufficiency. Diabetic glomerular sclerosis and terminal septic shock in one patient accounted per se for the urinary findings and terminal oliguric renal failure. In the remaining 8 patients the renal abnormalities are interpreted as manifestations of Legionnaires' disease: these were acute renal insufficiency in 6, requiring dialysis treatment in 4, proteinuria in 7, hematuria in 5, leukocyturia in 5 and cylindruria in 3 patients. One patient died of pneumonia and one patient, without Legionella-related renal involvement, of septic shock. Renal histology of 5 patients showed acute interstitial nephritis in one and diffuse sclerosing interstitial nephritis in a second patient, whose biopsy was obtained after 3 months' hemodialysis treatment. In 3 patients renal biopsy findings were explained by preexisting renal pathology, i.e. diabetic nephropathy, chronic transplant rejection and shock kidney respectively. Renal failure requiring hemodialysis and urinary abnormalities were largely reversible.
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PMID:[Renal involvement in Legionnaires' disease]. 381 99

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.
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PMID:Effects of low-protein diet on experimental diabetic nephropathy in the rat. 390 11

Adhesion molecules are important for immune regulatory mechanisms concerning antigen presentation, lymphocyte activation, localisation and migration as well as effector-target cell interactions in inflammatory processes. The immunohistochemical expression of ICAM-3, a recently cloned new member of the immunoglobulin family which also binds leucocyte function antigen 1 (LFA-1), was examined in 80 needle core biopsies from 35 renal allografts, 7 patients with mesangioproliferative glomerulonephritis, 5 patients with extracapillary glomerulonephritis, 4 patients with interstitial nephritis and 5 patients with diabetic nephropathy and 20 normal kidneys. In all types of lesions ICAM-3 was constitutively expressed on the majority of infiltrating leucocytes without detectable upregulation or presentation on possible target structures during inflammation indicating its possible role to be mainly in initiation of the inflammatory response.
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PMID:Expression of the intercellular adhesion molecule-3 (ICAM-3) in human renal tissue with relation to kidney transplants and various inflammatory diseases. 757 78

A strong familial clustering of ESRD has been reported among African Americans, suggesting that factors predisposing to renal failure, whether genetic, environmental, or both, may disproportionately affect certain families. A case-control study was undertaken to determine if a familial risk of ESRD was present among white Americans, if this risk differed among causes of ESRD, and if variability in age at onset was attributed to familial factors. Data were obtained from 103 white American patients (cases) with ESRD receiving dialysis treatments at the Bowman Gray School of Medicine's affiliated dialysis facility in Winston-Salem, NC. One hundred three age-, sex- and race-matched non-ESRD controls were consecutively selected from the Wake Forest University Physicians internal medicine clinic. Odds ratios (OR) and associated 95% confidence intervals (CI) were calculated to signify the prevalence of a relative with ESRD among cases versus controls. The presence of either a first- or second-degree relative increased a white American's risk for developing ESRD nearly threefold (OR = 2.7, 95% CI 1.1 to 7.2; P = 0.038), whereas the presence of either a first-, second- or third-degree relative with ESRD increased the risk nearly fourfold (OR = 3.5, 95% CI 1.5 to 8.4; P = 0.004). Cases with chronic glomerulonephritis and Type II diabetic nephropathy as the cause of ESRD had relatives with ESRD more often than cases with Type I diabetic nephropathy, interstitial nephritis, or renal artery stenosis. The average correlation (f) of ages at onset of ESRD among individuals in a single family (cases and their relatives) was 55%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Familial risk, age at onset, and cause of end-stage renal disease in white Americans. 778 48


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