pituitrin and Cardio-Renal-Syndrome

The authors summarize some current views regarding the pharmacologic therapies of hepatorenal and cardiorenal syndromes, respectively. A common pathogenetic background of the two edematous disorders is outlined, consisting in reduced effective blood arterial volume ‑ due to the splanchnic vasodilation in the hepatorenal syndrome (HRS) and to the fall in cardiac output and the rise in central venous pressure in cardiorenal syndrome (CRS). In both diseases, arterial underfilling elicits multiple water- and sodium- retentive mechanisms, by activating sympathetic nervous system and stimulating both rennin-angiotensin-aldosterone and vasopressin systems. These neurohormonal adjustments subsequently concur to a vasomotor nephropathy which originates - as a same kind of vasoconstrictor reflex renal response ‑ from the splanchnic vasodilation, in the case of liver cirrhosis, or from the fall in renal perfusion and filtration gradients in the case of cardiorenal syndrome. Despite these pathogenetic similarities, the renal insufficiency of HRS compared to that of CRS is treated using diametrically opposite approaches: actually withdrawal of diuretics and administration of vasoconstrictor agents is the first choice in the case of HRS, while CRS is tackled by forcing diuretic regimen and by continuing vasodilator treatment with ACE-inhibitors. The pros and cons of these strategies ‑ which are still matter of debate among the physicians and researchers ‑ are then succinctly presented and discussed.

Topics: Angiotensin-Converting Enzyme Inhibitors; Cardiac Output, Low; Cardio-Renal Syndrome; Diuretics; Hepatorenal Syndrome; Humans; Renin-Angiotensin System; Vasoconstrictor Agents; Vasodilation; Vasodilator Agents; Vasopressins

Obestatin regulates fluid and electrolyte homeostasis mainly by opposing the action of vasopressin (AVP). We measured plasma concentration of obestatin and AVP in patients with cardiorenal syndrome (CRS). Plasma AVP and obestatin concentration were measured in 34 patients with type II CRS. The data were compared to that in 31 patients with chronic kidney disease (CKD), 41 patients with chronic heart failure (CHF) and 30 healthy subjects. Obestatin was significantly higher in the patients with CRS (355.8 ± 85.1 pg/ml) than that in the healthy controls (212.3 ± 37.9 pg/ml, P<0.01), the patients with CKD (246.7 ± 34.3 pg/ml, P<0.01) and the patients with CHF (258.4 ± 112.1 pg/ml, P<0.01). AVP was also significantly higher in the patients with CRS (65.1 ± 36.0 pg/ml) than that in the healthy controls (38.5 ± 20.1 pg/ml, P<0.01), the patients with CKD (50.4 ± 24.8 pg/ml, P<0.01) and the patients with CHF (54.6 ± 16.3 pg/ml, P<0.01). Plasma concentration of obestatin was positively correlated with AVP plasma concentration in the overall analysis that included subjects from all disease categories (r = 0.219, P<0.05), but not within the CRS group. Plasma obestatin and vasopressin were elevated in patients with CRS. Plasma obestatin concentration seemed to be positively correlated with plasma AVP.

Topics: Cardio-Renal Syndrome; Female; Ghrelin; Humans; Male; Middle Aged; Vasopressins