Post-renal acute renal failure

A 54-year-old Hispanic man with type 2 diabetes mellitus and hypertension was initially evaluated at another institution for difficulty voiding urine. He was found to have a serum creatinine of 7.1mg/dl that had increased from his baseline of 1.0mg/dl 2 years earlier. Renal ultrasound revealed bilateral hydronephrosis with hydroureter. In addition, he had significant enlargement of his prostate. Over the ensuing 4 months, he underwent three transurethral resections of his prostate for persistent symptoms. His serum creatinine plateaued at 3.8mg/dl. He was referred to our institution for further evaluation and management of his persistent symptom of voiding difficulty and elevated creatinine. At our institution, a detailed history and physical examination was performed. His International Prostate Symptom Score (IPSS) was 35, suggesting severe lower urinary tract symptoms. 1 He denied poly- or oliguria, dysuria, fever, chills, and change in weight or appetite. His medications included NPH insulin and amlodipine. He denied tobacco, alcohol, and occupational chemical exposure, exposure to asbestos, tuberculosis, or use of over-the-counter medications. His family history was not significant. Physical examination revealed a well appearing man with blood pressure of 126/80mm Hg, body mass weight 34 kg/m(2). Jugular venous pressure was 9cm H2O, lungs were clear to auscultation, cardiovascular exam revealed a displaced left ventricle apical impulse, the abdomen was obese, non-tender with no palpable kidneys, and prostate enlargement on digital rectal exam. Examination of the testicles was unremarkable. Extremities did not reveal edema or changes of chronic venous stasis. Normal dorsalis pedis pulses were present on palpation. Renal ultrasound revealed mild bilateral hydronephrosis and hydroureter. Urodynamic measurements showed no evidence of outlet obstruction. A trial of indwelling urinary catheter was without benefit. Magnetic resonance imaging of the abdomen showed fibrosed soft tissue in the retroperitoneum, narrowing of the inferior vena cava and hydronephrosis consistent with retroperitoneal fibrosis (Figure 1a). Serology revealed an elevated acute-phase reactants 126mm/h, auto-antibodies 1: 160 (speckled), and a positive anti-ribonucleo protein (anti-RNP) assay. Investigation for secondary causes was undertaken. Extensive drug history did not reveal any medications that could cause retroperitoneal fibrosis (e. g., methysergide, ergot derivatives, hydralazine, or beta-blocker). There was no history of trauma, radiation, or malignancy. Purified protein derivative test was negative. Prostate-specific antigen was 1.1mg/dl (within normal limits). Therefore, the diagnosis of idiopathic retroperitoneal fibrosis (IRF) was presumptively made.