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

Renal tissues from 37 patients with glomerulopathies involving glomerular crescents were investigated using an immunofluorescence technique. Immunohistologic findings revealed two kinds of crescents, those with fibrinogen deposits (active), and those without (inactive). The degree of IgG deposition in glomeruli with active crescents was much higher than in glomeruli with inactive crescents in acute glomerulonephritis (AGN) and chronic glomerulonephritis (CGN). Active crescents were observed only in biopsy specimens taken within three months after the onset of acute glomerulonephritis or the acute exacerbation of chronic glomerulonephritis. These findings suggest that in AGN and CGN active crescents occur in an earlier stage of glomerular lesions and a more active stage in the immunological process than inactive crescents. The significance of active crescents in SLE, diabetic nephropathy and nephropathy associated with rheumatic arthritis was not evaluated due to the small number of patients.
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PMID:Immunohistologic findings in the glomerular crescents in various renal diseases. 37 95

The renal microvasculature was examined stereoscopically after intraarterial injection of silicone rubber. Specimens studied were: 29 cases of normal kidney, 4 cases of sclerotic kidney, 10 cases of acute renal failure, and 10 cases of chronic renal failure from the final stage of chronic glomerulonephritis, malignant nephrosclerosis, diabetic nephropathy, and cortical necrosis. The following were common evidences for chronic renal failure: much reduction and wide deficiencies of filling in the cortex, increased filling of vasa recta, narrowing and spiralling of interlobular arteries and cortical afferent arterioles, appearance of giant glomeruli, rarefaction of the peritubular capillary plexus, and relative preservation of glomeruli in the juxtamedullary zone and vasa recta in the medulla may be the major pathway, after the interlobular arteries and afferent arterioles in the subcapsular cortex are destroyed, and these vascular architectural changes may be intimately related to the pathophysiology of chronic renal failure.
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PMID:Renal microvasculature in chronic renal failure. 106 90

ACE inhibitors which till recently were used only in the treatment of cardiovascular diseases are becoming a perspective group of drugs also in the treatment of chronic nephropathies. It was revealed that they are effective in particular in the treatment of proteinuria of different etiology and have also a marked renoprotective effect and are therefore recommended to slow down the progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard the progression of chronic glomerulonephritis and diabetic nephropathy. It may be excepted that their therapeutic application will in the near future be extended also to clinical nephrology.
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PMID:[ACE inhibitors--a prospective new group of drugs for the treatment of kidney diseases]. 129 14

The incidence of end-stage renal disease is increasing and this results in an enhanced requirement of renal replacement therapy facilities. This brings about a significant burden on health care budgets and makes strategies that slow down or even prevent deterioration of the renal function mandatory. Although large scale randomized, controlled and prospective clinical trials on the effect of blood pressure control on the course of renal function are lacking, there is circumstantial evidence from animal, epidemiological and clinical studies to state that treatment of hypertension to blood pressure values well within the normal range is most important to ameliorate the downhill course of renal function in patients with chronic renal failure. Moreover, treatment of hypertension is critical to reduce morbidity and mortality of cardiovascular disease in these patients, who have an increased risk for such events. Low-protein diets, if possible with ketoacid supplement, are advocated to slow down the deterioration of renal function. However, based on the results of recent studies, low-protein diets may only have a moderate effect in patients with diabetic nephropathy and, possibly, in patients with chronic glomerulonephritis. The possibility of influencing renal ammoniagenesis by protein restriction or calcium carbonate administration, and an attenuation of alternative complement pathway activation and tubulo-interstitial injury, are challenging. Finally, in animal studies it has been found that abnormalities in serum lipid profile contribute to the progression of chronic renal failure, which may be prevented by pharmacological treatment of hyperlipidemia. Studies in humans concerning this subject are lacking at this moment, but treatment of hyperlipidemia is proper to reduce cardiovascular events.
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PMID:Clinical strategies for arresting progression of renal disease. 140 61

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.
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PMID:The pathological basis of chronic renal failure in Nigerians. An autopsy study. 149 21

Three cases of combined heart and kidney transplantation are presented. All three patients suffered from end-stage kidney disease, one chronic glomerulonephritis, two diabetic nephropathy. Ages of the patients were 22, 30, and 39 years, respectively. Two of the patients had the diagnosis of dilated cardiomyopathy and the third had ischemic heart disease. Patient follow-up is from 6 to 30 months. None of the patients have had a heart rejection and only one has had a kidney rejection. Cardiac and renal function remain excellent in all three patients. Glomerular filtration rates range from 53 to 77 ml/min. These three cases are compared with other reported cases in the literature. Combined heart and kidney transplantation may be of benefit in selected persons.
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PMID:Simultaneous heart and kidney transplantation: a report of three cases and review of the literature. 154 Jun 4

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

It is well known that urinary FDP is one of the parameters of intrarenal coagulation in renal disease. The measurement of urinary FDP, however, is not satisfactory enough, since it is not a quantitative and sensitive method. Latex photometric immunoassay has recently been developed as a quantitative and more sensitive method. Since fibrinogen reacts with FDP-E less than FDP, the measurement of urinary FDP-E is much better than that of urinary FDP in order to determine the presence of intrarenal coagulation and fibrinolysis of patients with renal diseases. The aim of this study is to clarify the clinical significance of urinary FDP-E measured by LPIA in the renal disease. The results were as follows: (1) Urinary FDP-E correlate with urinary protein, FDP, FDP-D, fibrinopeptide A (FPA), but not serum FDP-E. (2) The diseases which showed higher amounts of urinary FDP-E were diabetic nephropathy, amyloidosis and chronic glomerulonephritis. On the other hand, the diseases which showed smaller amounts of urinary FDP-E were minimal change, toxemia of pregnancy and lupus nephritis. All patients with higher amounts of urinary FDP-E showed marked renal dysfunction. But all the patients with the marked renal dysfunction did not always show higher amounts of urinary FDP-E. The urinary FDP-E showed a positive correlation to 1/serum creatinine. These results suggested that the measurement of urinary FDP-E is a useful method in determining the presence and degree of intrarenal coagulation and fibrinolysis in renal diseases.
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PMID:[Clinical significance of urinary FDP-E measured by latex photometric immunoassay (LPIA) in the renal disease]. 187 56

Activation of fibrinolysis in patients with diabetic nephropathy was determined by the plasma levels of plasmin-alpha 2 plasmin inhibitor complexes (alpha 2PIC) using a one-step sandwich enzyme immunoassay (EIA). Plasma levels of alpha 2PIC in diabetic patients with persistent proteinuria were significantly higher than those in diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Plasma levels of alpha 2PIC in diabetic patients with intermittent proteinuria were also significantly higher than those of diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Diabetic patients have been suggested to have a hypercoagulable state. The findings obtained from this study indicated that activation of fibrinolysis might counteract the hypercoagulable state in patients with diabetic nephropathy.
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PMID:Fibrinolysis in patients with diabetic nephropathy determined by plasmin-alpha 2 plasmin inhibitor complexes in plasma. 215 Dec 30


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