Association of Podometric Findings in Patients With Hypertension and Type 2 Diabetes: A Retrospective Analysis
Christopher Paschen1, Maximilian C Koeller2, Helga Schachner2
1Division of Nephrology and Dialysis, Department of Medicine III (C.P., K.D., M.K., M.H., R.O.), Medical University of Vienna, Austria.
Background:
Arterial hypertension (HTN) and type 2 diabetes (T2DM) are contributors to chronic kidney disease leading to glomerulomegaly and podocyte loss. Enlarged glomeruli and podocyte depletion are associated with kidney disease progression. This retrospective study aimed to investigate morphometric changes in patients with HTN and the contribution of coexisting T2DM in HTN.
Methods:
Glomerular and podocyte structure was estimated stereologically in unaffected areas of tumor nephrectomies in 99 patients. Morphometric features between subjects with HTN (n=47), HTN+T2DM (n=32), and controls without HTN and T2DM (n=20) were compared by ANOVA. Linear regression models evaluated the effect of morphometric parameters on renal compensation after nephrectomy (change of estimated glomerular filtration rate from pre-nephrectomy to 12 months post-nephrectomy).
Results:
In total, 36% of the HTN and 50% of the patients with T2DM exhibited dipstick-positive proteinuria. Glomerular volume in HTN+T2DM was similar compared with controls (2.7±0.8 versus 2.3±0.8×106 µm³; P=0.16) and to HTN only (2.7±0.9×106 µm³; P=0.95). Podocyte density was reduced in HTN+T2DM versus controls (217±66 versus 279±75 per 106 µm³; P=0.02) and not different to HTN only (233±87 per 106 µm³; P=0.67). Podocyte nuclear volume was larger in HTN+T2DM versus controls (230±28 versus 201±32 µm³; P=0.004) and similar to HTN (221±33 µm³; P=0.39). Larger glomerular volume (P=0.009), reduced podocyte density (P=0.003), and nuclear hypertrophy (P=0.01) were associated with impaired compensation.
Conclusion:
The patterns of podocyte depletion and nuclear hypertrophy were independently observed in both HTN and HTN+T2DM versus controls. Coexisting T2DM exhibited no additional contribution to glomerular and podocyte alterations.
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