Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis

To investigate the role of nitric oxide (NO) with respect to kidney function and liver cirrhosis, we evaluated renal function, as well as cyclic guanosine monophosphate (cGMP) and NOx (nitrite/nitrate [NO3− /NO2−]) as indirect markers of NO formation in plasma and urine at rest and during amino acid (aa)‐induced glomerular hyperfiltration in patients with Child A liver cirrhosis and portal hypertension (n = 12), and in healthy controls (n = 10). Baseline filtration rate (GFR) and effective renal plasma flow (ERPF) were significantly lower in patients with cirrhosis than in controls (GFR: mean 88 ± SD 16 mL/min vs. 106 ± 15 mL/min, P = .01, ERPF: 477 ± 93 vs. 561 ± 72 mL/min, P = .002). In both groups amino acid (aa) infusion increased GFR, ERPF, as well as cGMP and urinary NOx. Changes in GFR were similar in cirrhotic patients and controls (28.3% ± 14% in cirrhotics and 26% ± 11% in controls), but the degree of aa‐induced changes in ERPF was more marked in patients with liver cirrhosis (31.8% ± 17% vs. 18.6% ± 12%, P = .02). Plasma levels of NOx and cGMP were similar in either group at baseline and during aa infusion, whereas NOx and cGMP excretion in cirrhotics was constantly 14% to 24% lower than in the control group. We conclude that patients with compensated liver cirrhosis and portal hypertension already have an impaired kidney function. In addition our data suggest a cirrhosis‐related dissociation between ERPF and GFR during aa stimulation. Further studies are warranted to find out whether a local imbalance between vasoconstrictors and vasodilators, e.g., decreased local NO formation, plays a key role for this phenomenon.