Effect of chronic renal failure and hemodialysis on carbohydrate metabolism.

Hampers, Constantine L.; Soeldner, J S; Doak, P. B.; Merrill, John P.

doi:10.1172/jci105478

Cited by 203 publications

(69 citation statements)

References 25 publications

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“…The The importance of altered tissue responsiveness to ision of gluca-glucagon in uremia is underscored by the differential infusion rate in effects of dialysis on glucose tolerance and plasma glune response in e consequently cagon levels. Although, in according with previous mbined in the reports (5,(9)(10)(11)(12), dialysis was associated with an imf the changes provement in glucose tolerance (Fig. 4), plasma glu-L1 subjects (at cagon levels remained unchanged.…”

Section: Discussionsupporting

confidence: 76%

“…Improvement in asplanted dog glucose tolerance after chronic dialysis is associated tory reveal a with a return of glucagon sensitivity to normal. It tss the kidney should be noted that previous studies involving bolus induction of injections of 0.15-1.0 mg of glucagon have shown a tent renal up-variable glucose response to glucagon in uremic paFurthermore, tients (1,2,5,33). However, the data on the BSDRG ation (14) in glucagon (less than 2 ng/kg per min in both the Lgon.…”

Section: Discussionmentioning

confidence: 95%

“…The role of insulin resistance in the pathogenesis of the carbohydrate intolerance in uremia has recently been emphasized (4). Decreased sensitivity to the hypoglycemic effects of endogenous (2,5,6) and exogenous (3,(5)(6)(7)(8) insulin has been observed in uremic man, whereas basal and glucose-stimulated insulin concentrations are normal or increased (1-3, 5, 6, 9). After chronic dialysis, glucose tolerance generally improves in association with increased tissue sensitivity to insulin (5,(9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

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Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

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A B S T R A C T To evaluate the mechanism and role of hyperglucagonemia in the carbohydrate intolerance of uremia, 19 patients with chronic renal failure (12 of whom had undergone chronic hemodialysis for at least 11 mo) and 35 healthy control subjects were studied. Plasma glucagon, glucose, and insulin were measured in the basal state, after glucose ingestion (100 g), after intravenous alanine (0.15 g/kg), and during a 3-h continuous infusion of glucagon (3 ng/kg per min) which in normal subjects, raised plasma glucagon levels into the upper physiological range.Basal concentrations of plasma glucagon, the increment in glucagon after infusion of alanine, and postglucose glucagon levels were three-to fourfold greater in uremic patients than in controls. The plasma glucagon increments after the infusion of exogenous glucagon were also two-to threefold greater in the uremics. The metabolic clearance rate (MCR) of glucagon in uremics was reduced by 58% as compared to controls. In contrast, the basal systemic delivery rate (BSDR) of glucagon in uremics was not significantly different from controls.Comparison of dialyzed and undialyzed uremics showed no differences with respect to plasma concentrations, MCR, or BSDR of glucagon. However, during the infusion of glucagon, the increments in plasma glucose in undialyzed uremics were three-to fourfold greater than in dialyzed uremics or controls. When the glucagon infusion rate was increased in controls to 6 ng/kg per min to produce increments in plasma glucagon comparable to uremics, the glycemic response remained approximately twofold greater in the undialyzed uremics. The plasma glucose response to glu- cagon in the uremics showed a direct linear correlation with oral glucose tolerance which was also improved with dialysis. The glucagon infusion resulted in a 24% reduction in plasma alanine in uremics but had no effect on alanine levels in controls. It is concluded that (a) hyperglucagonemia in uremia is primarily a result of decreased catabolism rather than hypersecretion of this hormone; (b) sensitivity to the hyperglycemic effect of physiological increments in glucagon is increased in undialyzed uremic patients; and (c) dialysis normalizes the glycemic response to glucagon, possibly accounting thereby for improved glucose tolerance despite persistent hyperglucagonemia. These findings thus provide evidence of decreased hormonal catabolism contributing to a hyperglucagonemic state, and of altered tissue sensitivity contributing to the pathophysiological action of this hormone.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

View full text Add to dashboard Cite

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“…Many of the abnormalities present in patients with chronic renal disease such as anemia (32), hypertension (33), glucose intolerance (34), thrombocytopenia (35), encephalopathy (36), and polyneuropathy (37) (33,38). These observations are consistent with our findings that hemodialysis (T.D., Tables I, II, III, V) in contrast to homotransplantation (J. P. and C.M., Tables I, II, III, V) was ineffectual in altering the deranged metabolism of vitamin D,.…”

Section: Resultsmentioning

confidence: 99%

The metabolic fate of vitamin D3-3H in chronic renal failure

Avioli¹,

Birge²,

Lee³

et al. 1968

J. Clin. Invest.

161

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A B S TRA CT The absorption and metabolism of vitamin D3-3H was studied in eight patients with chronic renal failure. Although the intestinal absorption of vitamin D8-3H was normal, the metabolic fate of the vitamin was abnormal as characterized by a twofold increase in fractional turnover rate, an abnormal accumulation of biologically inactive lipid-soluble metabolites, and the urinary excretion of both vitamin D3-3H and biologically inactive metabolites. Neither alterations in watersoluble vitamin D. metabolites nor qualitative abnormalities in protein-binding of vitamin D.were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D, metabolism and excretion, renal homotransplantation was completely successful in this regard, These experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronic renal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of vitamin D. INTRODUCTIONThe occurrence of skeletal abnormalities in patients with chronic renal disease (renal osteodystrophy) and the destructive effects of secondary hyperparathyroidism and chronic acidosis on bone in uremia have been well established (1-5). Recent observations by Dent, Harper, and Philpot (2) and Stanbury and Lumb (3,4) suggest that renal

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“…However, it has not been conclusively demonstrated that this might happen within the ARF patients undergoing haemodialysis in critical care. In addition, longer post-dialysis duration would likely show significant change in S I , but 10 to 15 hours of investigation post-dialysis would be impossible to segregate changes in S I from other issues and dysfunction of critical illness (Hampers et al, 1966). Thus, a substantial change in S I at OFF/ON transition indicates a continuous and fast process of cleaning and clearing waste substances from blood.…”

Section: Discussionmentioning

confidence: 99%

Observation of changes in model-based insulin sensitivity during haemodialysis transitions for critically ill patients

Jamaludin

Docherty

Chase

et al. 2012

IFAC Proceedings Volumes

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Most critically ill patients exhibit a myriad of symptoms with irregular glycaemic regulation and renal failure contributing to a large proportion of mortality and morbidity. Hence, the effect of dialysis on glycaemic regulation should be of interest to clinicians as it is a common therapy addressing renal failure.In this investigation, we measure transient changes in model-based insulin sensitivity during the commencement and end of dialysis periods in 51 critically ill patients with acute renal failure (ARF). The clinically validated model-based insulin sensitivity (S I ) metric is a lumped parameter, which, in this case, can account for variance in insulin pharmacokinetics and production, as well as the efficiency of insulin mediated glucose uptake. Apparent S I is expected to be higher during renal failure as insulin will not be cleared as fast as the model assumed. Thus, it is hypothesized given model assumptions on steady, population levels of renal insulin clearance, that dialysis will cause a drop in model-based S I , and vice versa. This study is the first to investigate the effect of dialysis on insulin action of critically ill patients.This investigation found a significant reduction in model-based S I after the commencement of dialysis, but an insignificant change when dialysis was stopped. As dialysis was considered to have little effect on true insulin sensitivity and the effect on insulin production would have been contrary to the observed behavior, it was concluded that commencing dialysis had a significant effect in increasing insulin clearance over the cohort. This effect was not reciprocated immediately following dialysis due to a slower return to complete renal failure following treatment.

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Effect of chronic renal failure and hemodialysis on carbohydrate metabolism.

Cited by 203 publications

References 25 publications

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

The metabolic fate of vitamin D3-3H in chronic renal failure

Observation of changes in model-based insulin sensitivity during haemodialysis transitions for critically ill patients

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