Pathophysiology of Ischemic/ Toxic Acute Renal Failure

Andreucci, Vittorio E.

doi:10.1007/978-1-4613-2841-4_1

Cited by 8 publications

(2 citation statements)

References 186 publications

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“…The American Heart Association (AHA) guidelines [ 20 ] and the European Resuscitation Council Guidelines [ 21 ] recommend 10 U regular insulin and 25 g glucose intravenous over 15 to 30 minutes, but in studies insulin dosage ranged from 5 to 10 U and glucose from 25 to 60 g [ 22 ]. Other protocols include a second dose of 25 g glucose intravenously 60 minutes after the administration of the AHA guideline regimen to prevent hypoglycemia [ 13 ], the use of insulin aspart instead of insulin regular with a variable dose of glucose [ 14 ], the administration of a bolus of 5 U of insulin to be repeated every 15 minutes plus a 50 g/h glucose infusion [ 23 ], the use of a higher amount of insulin and glucose over a longer period of time [ 24 ] or even an insulin-free regimen with only a glucose bolus as treatment [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function

et al. 2017

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BackgroundHypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non-dialysis dependent CKD patients who received an intravenous infusion of insulin plus glucose to treat hyperkalemia.MethodsWe retrospectively reviewed charts of all AKI and non-dialysis dependent CKD patients who received 10 U of insulin plus 50 g glucose to treat hyperkalemia from December 1, 2013 to May 31, 2015 at our Department.ResultsOne hundred sixty four episodes of hyperkalemia were treated with insulin plus glucose and were eligible for analysis. Serum potassium levels dropped by 1.18 ± 1.01 mmol/l. Eleven treatments (6.1%) resulted in hypoglycemia and two (1.2%) in severe hypoglycemia. A lower pretreatment blood glucose tended to associate with a higher subsequent risk of hypoglycemia. Age, sex, renal function, an established diagnosis of diabetes or previous treatment were not associated with the development of this complication. We did not register any significant adverse events.ConclusionOur intravenous regimen combining an infusion of insulin plus glucose effectively reduced serum potassium levels compared to previous studies and associated a low risk of symptomatic hypoglycemia and other complications.

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Section: Introductionmentioning

confidence: 99%

Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function

et al. 2017

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“…Secondly, detached tubular cells can cause tubular obstruction. Finally, at sites with a denuded basement membrane, the ultrafiltrate can leak back from the tubular lumen into the circulation (Andreucci, 1984).…”

Section: Introductionmentioning

confidence: 99%

Cisplatin effects on F-actin and matrix proteins precede renal tubular cell detachment and apoptosis in vitro

Kruidering

Zhan

et al. 1998

Cell Death Differ

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In primary cultures of porcine proximal tubular kidney cells and LLC-PK1 cells cisplatin (5 ± 50 mM) caused apoptosis and cell detachment; in both systems cell detachment occurred, preceded by a loss of cytoskeletal F-actin stress fibers within 4 ± 6 h, and a reduction of mRNA encoding for fibronectin, collagen a 2 type (IV) and laminin B2 within 17 ± 41 h. Prevention of F-actin damage by phalloidin prevented nuclear fragmentation, suggesting a relation between F-actin damage and apoptosis. Overexpression of Bcl-2 also prevented apoptosis, but did not prevent damage to the F-actin skeleton or the reduction of mRNA expression of the matrix proteins. These results suggest that Bcl-2 overexpression interferes with apoptotic signals downstream of F-actin. The relevance of these results for cell detachment in kidney toxicity is discussed.

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Startreaktionen des posttraumatischen Schocks — Reperfusionsschaden

Schlag¹,

Redl²

1990

53. Jahrestagung Der Deutschen Gesellschaft Für Unfallheilkunde e.V.

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Pathophysiology of Ischemic/ Toxic Acute Renal Failure

Cited by 8 publications

References 186 publications

Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function

Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function

Cisplatin effects on F-actin and matrix proteins precede renal tubular cell detachment and apoptosis in vitro

Startreaktionen des posttraumatischen Schocks — Reperfusionsschaden

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