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Calcium antagonists and renal protection
H H Neumayer1, J Gellert, F C Luft
1Department of Medicine and Nephrology University of Erlangen-Nürnberg, Germany.
Renal Failure
|January 1, 1993
Summary
Calcium antagonists offer renal protection by improving hemodynamics and blocking cellular damage. These agents may be valuable in preventing acute kidney injury from ischemia, contrast media, or nephrotoxic drugs.
Area of Science:
- Nephrology
- Pharmacology
- Cardiovascular Medicine
Background:
- Calcium antagonists demonstrate potential renal protective effects.
- Their ability to reverse renal vasoconstriction and block intracellular calcium overload is key.
- This protective action is relevant for acute renal insufficiency caused by ischemia, contrast media, or nephrotoxic drugs.
Purpose of the Study:
- To review the evidence supporting the renal protective effects of calcium antagonists.
- To explore the mechanisms by which calcium antagonists may ameliorate declining glomerular filtration rate (GFR).
- To highlight the potential role of calcium antagonists in managing acute and chronic renal insufficiency.
Main Methods:
- Review of existing literature and prospective, controlled studies.
- Analysis of clinical trials investigating calcium antagonists in renal transplantation and contrast-induced nephropathy.
- Examination of experimental data in animal models of renal insufficiency and hypertension.
Main Results:
- Calcium antagonists protected against postischemic acute renal failure in renal transplantation.
- Prophylactic nitrendipine reduced GFR decline in patients receiving radiographic contrast agents.
- Experimental studies support the renoprotective actions of calcium antagonists in various models.
Conclusions:
- Calcium antagonists show promise in ameliorating acute renal insufficiency.
- Their benefits may extend to chronic renal insufficiency, especially when complicated by hypertension.
- Proposed mechanisms include blood pressure reduction, anti-hypertrophic effects, and modulation of cellular processes.