Progressive Multiple Sclerosis Presenting With Obstructive Uropathy and Acute Kidney Injury: A Case Report.

Very-late-onset multiple sclerosis (VLOMS), defined as disease onset after the age of 60, is a rare and often diagnostically challenging entity that may present with atypical features. We describe the case of a 67-year-old man who presented with progressive urinary symptoms culminating in obstructive uropathy and acute kidney injury (AKI), ultimately diagnosed as progressive multiple sclerosis (MS). The patient had a three-year history of left upper limb weakness and gait difficulty, which had been previously unexplored. He presented acutely following a fall, with new-onset left-sided facial droop and worsening lower limb weakness. Laboratory investigations revealed severe hyperkalemia (serum potassium: 9.8 mmol/L), uremia, and elevated creatinine (731 µmol/L), indicating significant renal impairment (estimated glomerular filtration rate (eGFR): 7 mL/min/1.73 m²). Urinary tract imaging revealed bilateral hydronephrosis and a trabeculated bladder, suggestive of chronic urinary retention; the prostate was enlarged but without significant prostate-specific antigen (PSA) elevation. Catheterization led to immediate bladder decompression, and the patient received medical treatment for hyperkalemia. Neuroimaging (MRI brain and spine) revealed multifocal demyelinating lesions involving periventricular, temporal, pontine, and cervical cord regions, while a lumbar puncture confirmed the presence of oligoclonal bands in both CSF and serum. Neurological examination demonstrated upper motor neuron signs, including facial asymmetry, limb spasticity, and pyramidal weakness, further supporting a central nervous system etiology. Despite the presence of benign prostatic hyperplasia (BPH) and cervical spondylosis, the degree of neurological impairment, distribution of MRI lesions, and cerebrospinal fluid analysis collectively pointed to a diagnosis of progressive MS with neurogenic bladder dysfunction. This led to urinary retention, obstructive uropathy, and subsequent AKI. While lower urinary tract dysfunction is a common complication of MS, its initial manifestation as acute renal failure is rare, especially in patients without a prior diagnosis. This case highlights the diagnostic complexity in elderly patients where structural (BPH, spinal stenosis) and neurological causes may overlap. It also underscores the importance of a high index of suspicion for demyelinating disease in patients with unexplained bladder dysfunction, progressive motor deficits, and renal impairment. Early multidisciplinary involvement, including neurology, urology, nephrology, and rehabilitation, is essential for prompt diagnosis, bladder decompression, and prevention of irreversible renal damage. Long-term catheterization was instituted, with outpatient follow-up arranged to assess suitability for clean intermittent self-catheterization and continued neurological monitoring. This case illustrates that in older adults, especially men, attributing urinary symptoms solely to common urological conditions may overlook more insidious neurologic diseases such as MS. Timely recognition and appropriate intervention can significantly alter prognosis by preserving renal function and optimizing functional outcomes.