# Midodrine Monotherapy in Refractory Hepatorenal Syndrome-Acute Kidney Injury: A Case Report

## TL;DR

Midodrine monotherapy successfully improved kidney function in a patient with hepatorenal syndrome-acute kidney injury when standard treatments failed.

## Contribution

Demonstrates midodrine monotherapy as a viable alternative in refractory HRS-AKI cases.

## Key findings

- Midodrine monotherapy improved eGFR from 37 to 82 in one month.
- Renal function remained stable at 83 over one year after discontinuation.
- Patient was successfully weaned off midodrine before TIPS placement.

## Abstract

Hepatorenal syndrome-acute kidney injury (HRS-AKI) is a serious complication of advanced cirrhosis, often requiring vasoconstrictive therapy. Terlipressin with albumin is the first-line treatment; however, in cases of terlipressin failure or the unavailability of noradrenaline, alternative therapies are limited. Midodrine, typically used in combination with octreotide, has uncertain efficacy as monotherapy.

A 52-year-old woman with alcohol-related decompensated Child-Pugh B (CP-B) cirrhosis and severe portal hypertension developed HRS-AKI following a semi-elective umbilical hernia repair. Initial treatment with terlipressin and albumin led to partial resolution; however, renal function deteriorated on tapering and cessation. Noradrenaline was not feasible in the long term due to the need for central venous access, and the patient was unaccepting of long-term subcutaneous injections for octreotide + midodrine therapy. The patient was consequently started on midodrine 2.5 mg three times a day (TDS) and titrated to 10 mg TDS in conjunction with 20% albumin over the course of three days. Her renal function improved progressively over the course of two weeks, and she was discharged on midodrine 10 mg TDS. Follow-up over four months showed recovery in kidney function, and she was successfully weaned off midodrine therapy before proceeding to elective transjugular intrahepatic portosystemic shunt (TIPS) for her refractory ascites, leading to its complete resolution.

Midodrine in conjunction with octreotide is a common regimen for HRS-AKI where terlipressin or noradrenaline is not available or feasible. In our case, midodrine monotherapy improved renal function from an estimated glomerular filtration rate (eGFR) nadir of 37 to 82 in one month, remaining stable at 83 over one year later, with no recurrence of HRS post weaning of midodrine. While alpha-1 adrenergic agonists alone are not traditionally thought to overcome the splanchnic vasodilation seen in HRS, this case suggests otherwise. Our findings suggest a potential role for midodrine monotherapy as a treatment option in HRS-AKI refractory to standard vasoconstrictive therapy, where therapeutic options are limited due to the unavailability or lack of feasibility.