Carbohydrate Metabolism in Nephritis

Linder, G. C.; Hiller, Alma; Slyke, Donald D. Van

doi:10.1172/jci100014

Cited by 52 publications

(15 citation statements)

References 15 publications

(15 reference statements)

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“…In another case, M. R. (17), the administration of 5 to 10 grams of calcium chloride daily had a similar effect in increasing the ammonia-acid ratio, due to the excess excretion of ammonia over acid radicles. In this patient the pH and bicarbonate of the serum remained normal as a result of this compensatory mechanism.…”

Section: Van Slyke Linder Hiller Leiter Mcintoshmentioning

confidence: 88%

The Excretion of Ammonia and Titratable Acid in Nephritis

Slyke¹,

Linder²,

Hiller³

et al. 1926

J. Clin. Invest.

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As the result of past metabolic studies, especially those of Henderson and Palmer (12) it is known that the non-volatile acids produced in excess of fixed base by human metabolism are excreted in the urine in two forms, viz., as free acids, and as ammonium salts.Since the kidney is unable to form urine with a pH much lower than 5.0, it can excrete, in significant amounts, free acids of only the weak buffer type. In this class fall acid phosphates and the various organic adds. It appears, however, that free acid excretion may assist also in elimination of strong acids, which can react with buffer salts (e.g., HC + Na2HPO4 = H(NaHPO4) + NaCl), the free buffer acid being excreted in place of the strong acid. Thus Marriott and Howland (19)

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Section: Van Slyke Linder Hiller Leiter Mcintoshmentioning

confidence: 88%

The Excretion of Ammonia and Titratable Acid in Nephritis

Slyke¹,

Linder²,

Hiller³

et al. 1926

J. Clin. Invest.

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“…Les plus frappantes ont été trouvées chez des sujets atteints de pyélonéphrite et consistaient en une élévation des //-LP et des T G à jeun avec élévation anormale de ces frac tions lipidiques après ingestion d'un repas gras. Le fait que les anomalies soient beaucoup plus marquées au cours des pyélonéphrites qu'au cours des glomérulo néphrites suggère que la médullaire rénale joue peut-être un rôle dans le métabo lisme des lipides.Impaired glucose tolerance in patients with chronic renal insuffi ciency has long been known [18]. Investigations now seem to prove that peripheral decrease o f sensitivity to endogenous insulin is one o f the main factors responsible for this metabolic defect [1,6,10,27].…”

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Effects of Fat Load on Serum Lipids in Patients with Renal Disease

Kokot¹,

Kuska²,

E³

et al. 1971

Nephron

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As altered lipid metabolism was reported in patients with chronic renal failure, it was of value to establish the effect of fat loading on the concentration of total cholesterol (Ch), total fatty acids (TFA), β-lipoproteins (β-LP), triglycerides (TG) and free fatty acids (FFA) in serum. 194 patients with various renal diseases were examined. Abnormality in lipid handling was found not on y in uremic patients, but also in renal patients with unimpaired excretory kidney function. This abnormality was especially expressed in high fasting plasma levels of β-LP and TG in compensated pyelonephritic patients and in abnormal rise of these lipid fractions after ingestion of a fat meal. Lipid handling by compensated pyelonephritic patients was pathologically changed compared with glomerulonephritic subjects which seemed to indicate that the renal medulla might be connected with the lipid metabolism.

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“…Following recognition half a century ago of impaired glucose tolerance in patients with severe renal insufficiency [32], several ap proaches were pursued to determine the un derlying mechanism(s). Employing the socalled hyperinsulinemic euglycemic insulin clamp technique [33], which offers significant advantages over previous methods available for determination of tissue sensitivity to in sulin, it was established that the abnormal glucose tolerance is mainly and probably solely due to insulin resistance in peripheral tissues [34,35], i.e.…”

Section: Insulin Actionmentioning

confidence: 99%

End-Stage Renal Failure in Diabetic Nephropathy: Pathophysiology and Treatment

Schmitz¹,

Hansen²,

Ørskov³

et al. 1985

Blood Purif

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Forty percent of patients with insulin-dependent diabetes will develop nephropathy during the course of their disease, thus being the most important single disorder leading to end-stage renal failure (ESRF). Intensive metabolic control delays onset of diabetic nephropathy, the first omen of which is appearance of subclinical albuminuria, also termed microalbuminuria. Moreover, it is now established that intensive treatment of hypertension reduces rate of decline in GFR and thus postpones ESRF.When uremia eventually sets in, a range of biochemical and endocrine abnormalities can be included among those characteristics of diabetes mellitus per se. These include elevated plas ma levels of growth hormone, glucagon and free fatty acids, which may participate in the uremic insulin resistance superimposed on the preexisting diabetic carbohydrate intolerance.Hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) are two established modalities of renal replacement therapy in diabetes mellitus. Controlled clinical trials for comparison of CAPD versus HD treatment of diabetics are, however, still needed. The survival rate is approximately 80 and 65-95 % in insulin-dependent diabetic patients at 1 year during treatment with HD and CAPD, respectively. However, it is general experience that diabetics on CAPD exhibit a glycemic control, superior to that attained during HD. It has not been proved that patient survival after cadaveric renal transplantation is better than on dialysis. The degree of vascular heart disease seems to be the major determinant for survival of kidney-transplanted diabetic patients.

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Carbohydrate Metabolism in Nephritis

Cited by 52 publications

References 15 publications

The Excretion of Ammonia and Titratable Acid in Nephritis

The Excretion of Ammonia and Titratable Acid in Nephritis

Effects of Fat Load on Serum Lipids in Patients with Renal Disease

End-Stage Renal Failure in Diabetic Nephropathy: Pathophysiology and Treatment

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