Renal Histologic and Ultrastructural Findings in Psychogenic Polydipsia and Diabetes Insipidus

Abstract

The renal biopsies of 15 patients affected by polydipsia syndromes were examined under light and electron microscopes. The authors contend that the observed renal lesions (dilatation of the glomerular loops, tubular cell hypertrophy and vacuolization, and basal membrane swelling) are the morphologic result of tubular hyperfunction in the service of ion reabsorption. This, in turn, is secondary to the increased GFR.

Progranulin Deficient Mice Develop Nephrogenic Diabetes Insipidus

“…3B ) did not reveal signs of glomerulonephritis, tubulonephritis or tubulosclerosis. Overall, the kidney morphology agreed with the higher urine turnover [ 38 ], possibly owing to a vasopressin un-responsiveness, but without structural changes or diseases of the kidney that may result in renal water losses such as amyloidosis. Immune cell infiltration of the kidneys was not associated with higher plasma levels of the pro-inflammation markers, C-reactive protein ( Fig.…”

“…There was also no sign of osmotic diuresis due to excretion of glucose. Hence, the results point to a resistance of collecting tubules towards vasopressin resulting in a loss of aquaporin-2 expression and adaptive hypertrophy to handle the increased rates of glomerular filtration and tubular reabsorption that occur in models of central or nephrogenic diabetes insipidus [ 38 , 43 ].…”