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Hypertensive nephrosclerosis in African Americans versus Caucasians
Carmelita Marcantoni1, Li-Jun Ma, Charles Federspiel
1Division of Nephrology, University of Verona, Verona, Italy.
Insights
African Americans with hypertensive nephrosclerosis show a distinct, more severe pattern of kidney injury, particularly a solidified form of glomerulosclerosis. These findings suggest underlying genetic or microvascular factors contribute to differing disease mechanisms between racial groups.
Area of Science:
- Nephrology
- Pathology
- Hypertensive Nephropathy
Background:
- Hypertensive nephrosclerosis is a leading cause of kidney disease.
- African Americans exhibit higher rates of extensive glomerulosclerosis (GS) compared to Caucasians.
- The specific mechanisms and phenotypic differences in kidney injury between these groups remain unclear.
Purpose of the Study:
- To compare the severity and phenotype of kidney injury in African Americans and Caucasians diagnosed with hypertensive nephrosclerosis via renal biopsy.
- To investigate potential differences in the mechanisms of glomerular and interstitial damage between racial groups.
Main Methods:
- Retrospective analysis of renal biopsies diagnosed with hypertensive nephrosclerosis over 11 years.
- Semi-quantitative analysis of global and segmental glomerulosclerosis, interstitial fibrosis, and vascular sclerosis.
- Categorization of global glomerulosclerosis into solidified and obsolescent phenotypes.
Main Results:
- African Americans were younger, with higher creatinine, but similar blood pressure and proteinuria compared to Caucasians.
- African Americans showed significantly increased solidified glomerulosclerosis (25% vs. 8%) and interstitial fibrosis (54% vs. 33%).
- Solidified glomerulosclerosis was strongly associated with segmental sclerosis in African Americans, unlike in Caucasians.
Conclusions:
- Hypertensive nephrosclerosis presents with distinct morphological phenotypes in African Americans versus Caucasians.
- Blood pressure and proteinuria do not fully explain the observed differences, suggesting genetic or microvascular factors are involved.
- Different pathogenic mechanisms may underlie sclerosis development and progression in African Americans and Caucasians.
Background:
Extensive global glomerulosclerosis (GS) has been reported in African Americans with hypertension and renal insufficiency, far exceeding that in Caucasians. To assess and compare severity and phenotype of injury in biopsied African Americans and Caucasians who morphologically had hypertensive nephrosclerosis, we performed a retrospective biopsy study.
Methods:
All renal biopsies with a histological diagnosis of hypertensive nephrosclerosis from the last 11 years were identified from our clinical files. Lesions of global and segmental sclerosis, interstitial fibrosis and vascular sclerosis were semiquantitatively analyzed as percent involved, or on a 0 to 3 scale, respectively. The phenotypes of global glomerulosclerosis also were categorized as either the solidified (that is, the entire tuft is solidified) or the obsolescent type (that is, Bowman's space is occupied by collagenous material and the tuft is retracted).
Results:
Sixty-two patients (19 African Americans, 43 Caucasians) were included in the study. At biopsy, African Americans were younger than Caucasians with higher serum creatinine, but no difference in proteinuria or mean arterial pressure (MAP). African Americans had a marked increase in the solidified form of GS (25 +/- 6 in African Americans vs. 8 +/- 2% in Caucasians, P < 0.01). This extensive solidification of glomeruli was associated with segmental sclerosis in African Americans (38 +/- 10%), contrasting low prevalence of solidified GS in Caucasians with segmental sclerosis (10 +/- 3%, P < 0.05) and in African Americans without segmental sclerosis (10 +/- 4%, P < 0.05). African Americans with segmental sclerosis were younger and clinically expressed a more severe renal disease than Caucasians with this lesion. Interstitial fibrosis was greater in African Americans than in Caucasians (54 +/- 6 vs. 33 +/- 3%, P < 0.01) and correlated with proteinuria and serum creatinine levels, especially in African Americans, and also with GS. Vascular sclerosis was worse in African Americans than in Caucasians (0.96 +/- 0.04 vs. 0.77 +/- 0.08 score, P < 0.05) and did not correlate with GS. By modeling, neither MAP nor age was useful in predicting any morphological lesions and proteinuria accounted only minimally for the variability of GS.
Conclusions:
Blood pressure levels and proteinuria did not account for morphological lesions, suggesting other factors (such as genetic factors, microvascular disease) may play a role. The phenotype of GS differs in biopsied African Americans versus Caucasians with hypertensive nephrosclerosis, with a marked increase in the solidified form of GS in African Americans. The association of extensive solidified GS with segmental sclerosis lesions in African Americans, but not in Caucasians, suggests different mechanisms may contribute to the development and progression of sclerosis in these two patient groups.