Polycystic kidney disease natural history
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Natural History, Prognosis, and Complications
Natural History of Renal Manifestations
- The earliest detectable functional aberration seen in patients with ADPKD is impaired concentrating capacity with a suboptimal increase in urinary osmolality following water deprivation.[1]
- The second early manifestation of disease is hypertension. Up to 75% of patients with ADPKD on imaging without any renal insufficiency are hypertensive.[2] This is likely to be linked to an increase in the activity of the renin-angiotensin-aldosterone system (RAAS). RAAS overactivity is due to the increase in renin release secondary to renal ischemia brought on by cystic expansion and stretching of renal arterioles. This is further emphasized by the fact that patients with ADPKD generally respond better to ACE inhibitors and angiotensin receptor blockers than patients with essential hypertension.[3]
Natural History of Extra-renal Manifestations
References
- ↑ Gabow PA, Kaehny WD, Johnson AM, Duley IT, Manco-Johnson M, Lezotte DC; et al. (1989). "The clinical utility of renal concentrating capacity in polycystic kidney disease". Kidney Int. 35 (2): 675–80. PMID 2709672.
- ↑ Gabow PA (1990). "Autosomal dominant polycystic kidney disease--more than a renal disease". Am J Kidney Dis. 16 (5): 403–13. PMID 2239929.
- ↑ Chapman AB, Johnson A, Gabow PA, Schrier RW (1990). "The renin-angiotensin-aldosterone system and autosomal dominant polycystic kidney disease". N Engl J Med. 323 (16): 1091–6. doi:10.1056/NEJM199010183231602. PMID 2215576.