What is the most likely cause of oligoanuria in a 70-year-old diabetic and hypertensive male with no prior history of decreased urine output, presenting with difficulty breathing, tachycardia, tachypnea, and hyperkalemia, despite high fluid intake?

Acute Intrinsic Renal Failure (Acute Tubular Necrosis)

The most probable cause of oligoanuria in this patient is acute intrinsic renal failure, specifically acute tubular necrosis (ATN), precipitated by urinary tract infection in the setting of pre-existing chronic kidney disease from diabetes and hypertension. 1

Clinical Reasoning

This 70-year-old patient presents with severe acute kidney injury (creatinine 11 g/dL) and life-threatening complications including metabolic acidosis (pH 7.22, HCO3 8), severe hyperkalemia (K 6.7), and volume overload manifesting as pulmonary edema (bilateral rales, respiratory distress with RR 30s, neck vein distention) and peripheral edema. 1

Why This is Intrinsic Renal Disease (Not the Other Options):

Unilateral Obstructing Nephrolithiasis - EXCLUDED:

• Unilateral obstruction cannot cause oligoanuria unless the patient has a solitary functioning kidney, which is not mentioned in this case 1
• Postrenal causes account for less than 3% of AKI cases 1
• The urinalysis shows WBCs "too numerous to count" and RBCs 22/hpf with hyaline casts, which is more consistent with intrinsic renal disease than simple obstruction 1

Acute Prostatitis - EXCLUDED:

• While the patient has slight hypogastric distention, acute prostatitis alone would not cause bilateral mid-to-basal pulmonary rales, severe metabolic acidosis, or this degree of renal failure 1
• The urinalysis pattern (pyuria with hematuria and casts) suggests parenchymal kidney involvement, not simple bladder outlet obstruction 1

Neurogenic Bladder from Diabetes - EXCLUDED:

• Neurogenic bladder causes post-renal obstruction, which accounts for less than 3% of AKI 1
• The patient's severe volume overload (neck vein distention, pulmonary edema, peripheral edema) indicates the kidneys are retaining fluid rather than obstructing its outflow 1
• The metabolic derangements (severe acidosis, hyperkalemia) are disproportionate to what would be expected from simple urinary retention 1

Dehydration - EXCLUDED:

• The patient is drinking 2.5-3.0L of fluids daily and shows clear signs of volume overload: neck vein distention, bilateral pulmonary rales, and grade 2 pitting pedal edema 1
• Blood pressure is 130/90 (not hypotensive), arguing against prerenal azotemia 1
• The urinalysis shows specific gravity of 1.010 (isosthenuric), which indicates loss of concentrating ability consistent with intrinsic renal disease rather than the concentrated urine (specific gravity >1.020) expected in prerenal states 1

Supporting Evidence for Intrinsic Renal Disease (ATN):

Urinalysis Findings:

• WBCs "too numerous to count" indicates severe urinary tract infection, a known precipitant of ATN in diabetic patients 2
• Hyaline casts are consistent with acute tubular injury 1
• Specific gravity 1.010 (isosthenuric) indicates loss of concentrating ability, characteristic of intrinsic renal disease 1

Laboratory Pattern:

• The severe metabolic acidosis (pH 7.22, HCO3 8) with elevated anion gap suggests both lactic acidosis from tissue hypoperfusion and uremic acidosis from renal failure 3
• Severe hyperkalemia (6.7) in the setting of oliguria indicates impaired renal potassium excretion 3
• BUN 25 mg/dL with creatinine 11 g/dL gives a BUN:Cr ratio <20:1, which suggests intrinsic renal disease rather than prerenal azotemia 4

Clinical Context:

• Diabetes and hypertension are the predominant risk factors for chronic kidney disease, and this patient likely had underlying CKD that decompensated with the acute infection 1
• The urinary tract infection in a diabetic patient represents a nephrotoxic insult that precipitated ATN on top of chronic kidney disease 2
• The patient's attempt to increase fluid intake paradoxically worsened volume overload because the kidneys lost their ability to excrete sodium and water 1

Immediate Life-Threatening Issues Requiring Urgent Intervention:

This patient requires emergent hemodialysis for:

• Severe hyperkalemia (K 6.7) with risk of fatal arrhythmias 1
• Severe metabolic acidosis (pH 7.22) 1
• Volume overload causing respiratory failure (RR 30s, bilateral rales) 1
• Stage 3 AKI with oligoanuria meeting criteria for renal replacement therapy 1

The combination of severe hyperkalemia, metabolic acidosis, and pulmonary edema in the setting of oligoanuria represents a medical emergency with high mortality risk if dialysis is delayed. 1, 5