Diabetes insipidus is a polyuric disease characterized by excretion of a large volume of hypotonic urine and hypernatremia. It is due to the absence of antidiuretic hormone.
Central (hypothalamic or neurohypophyseal) diabetes insipidus is the inability to secrete & produce vasopressin in the neurohypophyseal system. It is due to damage to the pituitary gland & hypothalamus, may be due to diseases, head injuries, neurosurgery, infection or genetic or autoimmune disorders.
In nephrogenic diabetes insipidus, there is inappropriate renal response to vasopressin. Kidney function may be impaired by drugs & by chronic disorders like polycystic kidney disease, sickle cell disease, kidney failure, partial ureteral block, hypokalemia, hypocalcemia, low protein diet & genetic disorders.
Primary polydipsia have abnormal increase in fluid intake.
Measurements of arginine-stimulated copeptin can distinguish patients with central diabetes insipidus from those with primary polydipsia with an accuracy comparable to that of the hypertonic saline approach, the current diagnostic standard, according to a study. Furthermore, arginine stimulation is easier to perform and associated with fewer adverse effects.
Adding dapagliflozin to standard of care (SOC) significantly reduces the risk of worsening kidney function, death due to kidney or cardiovascular (CV) disease, and all-cause mortality compared with SOC alone in patients with chronic kidney disease (CKD), regardless of whether they have type 2 diabetes (T2D), reveals the DAPA-CKD* trial — showing dapagliflozin charting new territories from diabetes to the renal realm.
In patients with chronic heart failure with reduced ejection fraction (HFrEF), empagliflozin reduced the risk of cardiovascular (CV) death or heart failure hospitalization (HHF) and decline in estimated glomerular filtration rate (eGFR), results of the EMPEROR-Reduced* trial showed.