Sathish Obalanarasimhaiah1, Kiran Shankar2, Balakrishna Nanjundappa Setty3, Gnanendra Dibbadahalli Mariyanna4, Nagesh Nayakarahalli Swamigowda5, Parvesh Kumar Jain6
BACKGROUND
The increased propensity for acute kidney injury (AKI) in patients with cirrhosis
stems from haemodynamic abnormalities typical for patients with cirrhosis and
ascites.15 which is due to development of portal hypertension and portosystemic
collaterals with splanchnic and systemic vasodilatation, resulting in decrease in
effective arterial blood volume with increase in renin angiotensin-aldosterone
system (RAAS), sympathetic nervous system and non-osmotic release of
antidiuretic hormone causing sodium retention, increased intravascular volume,
and a hyperdynamic circulatory state,16 complemented with increased production
of nitric oxide which is considered the main cause of vasodilatation in cirrhosis.
Mechanism of renal dysfunction in cirrhosis includes portal hypertension & its
accompanying haemodynamic abnormalities15 leading to increased synthesis of
endogenous vasodilatory compounds such as nitric oxide leading to vasodilatation
in splanchnic & systemic arterial systems ultimately leading to activation of reninangiotensinogen–
aldosterone system causing compensatory renal
vasoconstriction & hypo-perfusion resulting into renal failure. We wanted to study
the clinical profile of patients with AKI who presented to a tertiary care hospital in
Bangalore.
METHODS
Ninety-four patients of either gender admitted in the department of
gastroenterology at a tertiary care hospital with age > 18 years with either
diagnosed or newly diagnosed case of cirrhosis of liver (including both
compensated & decompensated cases) admitted with acute kidney injury
diagnosed according to International Club of Ascites Classification were enrolled
in this study. The sample size was based on number of eligible patients admitted
to tertiary care hospital during the study period. Details of the study were
explained to them and consent was taken either from the patient or their attender.
RESULTS
Most patients were in the age group > 60 yrs. with 32 male patients (45.07 %) in
the age group of 40 - 60 years & 13 female patients (56.52 %) in the age group
of > 60 yrs. 78.7 % of patients developed AKI before hospital admission i.e., at
community level; whereas 21.3 % of patients developed AKI after hospital
admission i.e., they had normal creatinine level on admission.
CONCLUSIONS
Pre renal AKI was the most common cause of AKI followed by hepatorenal
syndrome & acute tubular necrosis (ATN) comprising 52.1 %, 28.7 % & 19.1 %
respectively.
