Case 3: Diagnosis & Conclusions

Case Published: June 2018

You order foley catheter placement, which results in an immediate 2.4 liters of urine output!


The patient begins to feel better, his mental status returns to baseline, and his creatinine rapidly downtrends. He is making a significant amount of urine, and you appropriately manage his post-obstructive diuresis using the guidelines below. As day of discharge approaches, you council the patient’s wife on his medications, optimize his glycemic control, and arrange close follow-up. Nice work!

Diagnosis: Urinary Tract Obstruction/Obstructive Nephropathy with Hydronephrosis

Case Summary:

This case presents us with a complex patient with many medical comorbidities that could have led to his acute kidney failure. The patient’s underlying chronic kidney disease puts him at increased risk for acute kidney injury (AKI). The key to this case is to determine which etiology is MOST likely and look for reversible causes!

Let’s briefly walk through the case. The patient presents with 3 days of nausea, vomiting, and altered mental status. This leaves us with a wide differential! An abbreviated list based on his history includes a gastrointestinal illness, medication side effects (newly started taking diphenhydramine), diabetic ketoacidosis, and even uremia. His vomiting could be a symptom of uremia or, alternatively, a cause of hypovolemia and “pre-renal” AKI. Without further investigation of this patient’s minimal urine output, his presentation could certainly be mistaken for isolated volume depletion.

The patient also has poorly controlled diabetes (hemoglobin A1c of 10.1%), raising concern for progression of diabetic nephropathy. However, the rise in creatinine to 12 from 2 in less than 1 month is acute.  Above all, this patient is at high risk for urinary tract obstruction (UTO) in the setting of poorly controlled diabetes that can be complicated by neurogenic (a flaccid or spastic) bladder. Further, recent initiation of a potent anticholinergic agent, diphenhydramine, increases suspicion for UTO. Anti-cholinergic medications reduce activity of the detrusor muscle, which allows the bladder to contract during urination.

This patient has a palpable bladder on examination, and the diagnosis of UTO is confirmed with new hydronephrosis on kidney ultrasound –  a finding with a positive predictive value of 70% when obstruction is suggested clinically. The patient’s hyperkalemia and acidosis are also suggestive of obstruction, which often results in a voltage-dependent type IV, or distal, renal tubular acidosis (RTA).

UTO can result from a variety of causes.
Our differential diagnosis includes:
*Prostatic disease (hyperplasia, cancer)
*Malignancy (metastatic or primary bladder/urinary tract)
*Neurologic (neurogenic bladder due to diabetes, spinal cord injury, etc.)
*Medication-induced retention, typically anti-cholinergic mediated
*Retroperitoneal fibrosis (progressive ureteral obstruction), which is very rare

UTO makes up approximately 10% of acute kidney injury and can occur anywhere along the urinary tract. When it leads to significant AKI, obstruction is often bilateral (or unilateral with a single functioning kidney or baseline impaired kidney function). Untreated, obstruction can lead to irreversible tubulointerstitial fibrosis.

Post-Obstructive Diuresis:

We can’t rest on our laurels once we make the diagnosis of UTO. Relief of the obstruction is the first step, whether this is by foley catheter, nephrostomy tubes, ureteral stent placement, or even tumor debulking depending upon the underlying etiology and patient’s anatomy. Once the flood starts, it’s time to get to work!

Even after initial relief of obstruction and an often high initial urine output, these patients usually continue to have a brisk urine output with up to several liters of urine output per hour.
Why do patients with UTO experience “post-obstructive diuresis”?
UTO leads to excess sodium and water retention as well as the accumulation of solutes such as urea. Once the obstruction is relieved, the patient will undergo an osmotic diuresis. Due to a combination of factors including perturbation of the medullary concentrating gradient, faster flow through the tubules (leaving less time for equilibration), decreased reabsorption of sodium in the tubules (due to disrupted expression of sodium transporters), and prostaglandin release, the patient may continue to have high urine output despite euvolemia or hypovolemia.

Without adequate fluid replacement, post-obstructive diuresis may result in severe hypovolemia and electrolyte derangements. Based on the available data, fluid replacement should be given with 0.45% normal saline to replace 75% of the urine losses (a good starting point is 0.5 cc/hr of fluid replacement per cc/hr of urine output) Electrolytes including potassium, magnesium, and phosphorus should be diligently monitored and repleted as needed. Resolution should begin in 1-2 days to a week. Remember to slowly decrease intravenous (IV) fluid administration as urine output slows down, as IV fluids will also drive urine output.

For more, take a look at the references below:

  1. Halbgewachs C, Domes T: Postobstructive diuresis: pay close attention to urinary retention. Can. Fam. Physician Med. Fam. Can. 61: 137–142, 2015
  2. Batlle DC, Arruda JA, Kurtzman NA: Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy. N. Engl. J. Med. 304: 373–380, 1981
  3. Klahr S: Obstructive nephropathy. Intern. Med. Tokyo Jpn. 39: 355–361, 2000
  4. Selius BA, Subedi R: Urinary Retention in Adults: Diagnosis and Initial Management. Am. Fam. Physician 77: 643–650, 2008
  5. Sparks M: Post obstructive diuresis [Internet]. Ren. Fellow Netw. 2010 Available from: [cited 2018 Jun 13]

Case 3 Index
Case 3 Introduction
Case 3 Physical Exam
Case 3 Diagnostic Testing
Case 3 Additional Testing