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[Risk factors for contrast nephropathy in diabetic patients undergoing cardioangiography]
1Department of Internal Medicine, Tohsei National Hospital, Shizuoka, Japan.
Insights
Diabetic patients with overt kidney disease are at higher risk for contrast nephropathy after cardioangiography. Tubular dysfunction, indicated by fractional excretion of sodium (FENa), is a key predictor of contrast-induced kidney injury.
Area of Science:
- Nephrology
- Cardiology
- Diabetology
Background:
- Contrast nephropathy is a significant complication following cardioangiography, particularly in diabetic patients.
- Diabetic nephropathy encompasses a spectrum of kidney damage, from early microalbuminuria to advanced overt proteinuria and declining glomerular filtration.
Purpose of the Study:
- To identify risk factors for contrast nephropathy in patients with non-insulin dependent diabetes mellitus undergoing cardioangiography.
- To determine the association between the stage of diabetic nephropathy and the development of contrast nephropathy.
Main Methods:
- Prospective study of 17 diabetic patients undergoing cardioangiography.
- Measurement of serum creatinine (Cr), fractional excretion of sodium (FENa), urinary albumin excretion rate (AER), and 24-hour creatinine clearance (Ccr) before and after angiography.
- Stepwise discriminant analysis to identify significant risk factors.
Main Results:
- Contrast nephropathy occurred in 29.4% of diabetic patients.
- Patients who developed contrast nephropathy had significantly higher Cr, FENa, AER, and lower Ccr.
- Contrast nephropathy was observed in all patients with overt proteinuria (AER > 200 µg/min) and three of seven with microalbuminuria.
- FENa before angiography was the most significant discriminant factor for contrast nephropathy (p = 0.0008).
Conclusions:
- Contrast nephropathy predominantly affects diabetic patients with advanced nephropathy, characterized by reduced glomerular filtration, overt proteinuria, and tubular dysfunction.
- Tubular dysfunction, as indicated by elevated FENa, appears to be the most critical risk factor for contrast nephropathy in this population.
Abstract:
Risk factors for contrast nephropathy were prospectively studied in 17 patients with non-insulin dependent diabetes mellitus undergoing cardioangiography. Contrast nephropathy, defined as a serum creatinine increase of greater than 25% at 3 day after angiography, occurred in 29.4% of diabetic patients. Patients who developed contrast nephropathy had significantly higher serum creatinine (Cr), fractional excretion of sodium (FENa), urinary albumin excretion rate (AER), and lower 24hr Ccr than patients who did not (Cr: 1.5 +/- 0.3 mg/dl vs. 0.8 +/- 0.1 mg/dl, FENa: 1.9 +/- 0.5% vs. 0.6 +/- 0.1%, AER: 522 +/- 335 micrograms/min vs. 27 +/- 13 micrograms/min, 24hr Ccr: 39.1 +/- 11.6 ml/min vs. 86.2 +/- 9.3 ml/min, P < 0.05). Contrast nephropathy developed in all of two patients with overt proteinuria (AER more than 200 micrograms/min), but none of eight patients with normoalbuminuria (AER below 15 micrograms/min). Three of seven patients with microalbuminuria developed contrast nephropathy, and two of them had advanced nephropathy. FENa obtained next day was significantly elevated over baseline in patients with contrast nephropathy (1.9 +/- 0.5% vs. 9.7 +/- 4.5%, P < 0.05), but unchanged in patients without contrast nephropathy. The rise in C beta 2-microglobulin/Ccr and enzymuria was noted in both group. Percentage decrease of Ccr on the next day was positively correlated with FENa before angiography (r = 0.645, p < 0.01). Of 24hr Ccr, AER, and FENa before angiography, FENa was revealed as a statistically significant discriminant factor for contrast nephropathy by stepwise discriminant analysis (p = 0.0008). These results suggest that contrast nephropathy develops predominantly in the stage not of incipient but of overt diabetic nephropathy indicated by a decline of glomerular filtration, overt proteinuria, and tubular dysfunction. Of them, tubular dysfunction may be the most important risk factor for contrast nephropathy.