Key result
Current knowledge about major genetic variants causing susceptibility to renal damage in hypertension is scarce, with many associations lacking replication across patient subgroups.
The review highlights that despite efforts in genetic studies, the major genetic variants responsible for renal damage in hypertension remain largely unconfirmed, necessitating larger replication cohorts.
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Current genetic associations do not support clinical risk prediction in hypertensive nephropathy; leaves open confirmation of major variants in larger replication cohorts.
Epidemiological as well as animal studies have recognized the potential role of genetic factors in the development of microalbuminuria and related traits (renal insufficiency, end-stage renal disease and nephroangiosclerosis) in hypertension. To unravel genetic variants of susceptibility, candidate gene, linkage and genome wide scan analysis has been used. In spite of the great efforts that have been made in the field, sound knowledge about the major genetic variants causing the susceptibility to develop renal damage in hypertension is scarce, since many associations were not replicated or only showed association in a certain subgroup of patients. Looking initially at genes of the most important physiological pathways of blood pressure regulation, linkage and genome wide scan have also detected genes of the lipid metabolism and protein components of the glomerular structures as potential candidate genes. Well designed large-scale genome-wide analysis and replication studies with large cohorts can help in the future to clarify the genetic bases of renal damage in hypertension. Combined strategies can contribute toward a better understanding of the genetic basis of urinary albumin excretion and renal damage in hypertension
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Martínez et al. (2010) conducted a review in Hypertension and renal damage. Genetic variants was evaluated on Urinary albumin excretion and related traits. Current knowledge about major genetic variants causing susceptibility to renal damage in hypertension is scarce, with many associations lacking replication across patient subgroups.
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