Diabetes insípida nefrogénica

Abstract

The anti-diuretic hormone arginine-vasopressin (AVP) is released from the pituitary and regulates water reabsorption in the principal cells of the kidney collecting duct. Binding of AVP to the arginine-vasopressin receptor type-2 in the basolateral membrane leads to translocation of aquaporin-2 water channels to the apical membrane of the principal cells of the collecting duct, inducing water permeability of the membrane. This results in water reabsorption in the collecting duct of the nephron following an osmotic gradient. Nephrogenic diabetes insipidus is caused by partial or complete renal resistance to the effects of AVP. Congenital nephrogenic diabetes insipidus is a disorder associated with mutations in either the AVPR2 or AQP2 gene, causing the inability of patients to concentrate their urine. Acquired nephrogenic diabetes insipidus can be caused by electrolyte imbalances (e.g., hypercalcemia, hypokalemia), renal/extra-renal diseases and drugs (e.g., lithium toxicity). This article reviews the causes, clinical manifestations, diagnosis and treatment of patients with nephrogenic diabetes insipidus. Based on more in-depth mechanistic understanding, new therapeutic strategies are current being explored.

Management of Nephrogenic Diabetes Insipidus: An Overview

“…Fluid intake is essential to prevent the harmful effect of repeated episodes of dehydration in nephrogenic diabetes insipidus. Due to the risk of developing highly distended urinary bladders due to polyuria, regular bladder emptying should be indicated to ensure that maximum bladder capacity remains within the normal range [28]. For example, infants with diabetes insipidus often cannot drink enough fluids to compensate for urinary losses.…”

“…In these cases, it is helpful to reduce the intake of sodium in the diet (1 mEq/kg/day) to reduce the solute load. In this population, it is not recommended to reduce protein intake as it can lead to malnutrition [28,29]. The primary strategy for managing NDI is to replace urinary water loss with adequate fluid supply in combination with a low-salt and low-protein diet to minimize obligatory water excretion.…”

The combined effect of hypomagnesemia and hypokalemia inducing nephrogenic diabetes insipidus in a patient with type 1 diabetes mellitus

“…This leads to polyuria of more than 3L in 24 hours with a urinary osmolality of less than 300 mOsm/kg H 2 O and specific gravity of less than 1.005, causing an increase in plasma osmolality in response to raised serum sodium and urea. 1,2 NDI can be hereditary or an acquired disorder. Acquired NDI is commonly caused by drugs such as lithium or metabolic imbalances, such as hypokalemia and hypercalcemia.…”

“…NDI results from the failure of the kidney to concentrate urine due to the insensitivity of the distal nephron to respond to antidiuretic hormone (ADH), also known as arginine vasopressin (AVP). This leads to polyuria of more than 3L in 24 hours with a urinary osmolality of less than 300 mOsm/kg H 2 O and specific gravity of less than 1.005, causing an increase in plasma osmolality in response to raised serum sodium and urea 1,2 …”

Coexistence of Central and Nephrogenic Diabetes Insipidus in a Preterm Infant

“…However, CDI in infants is rare, and has been associated to intraventricular hemorrhage, congenital infection, midline defects and septo-optic dysplasia [4]. Non-heritable causes of nephrogenic DI include primary tubulointerstitial nephropathies (polycystic kidney disease, hydronephrosis, renal tubular acidosis, idiopathic hypercalciuria) and secondary tubule-interstitial nephropathies (hypercalcemia and nephrocalcinosis, kaliopenic nephropathy, medication induced) [5].…”