Skip to content

Postrenal azotemia



Renal system


Renal and ureteral disorders
Bladder and urethral disorders
Renal system pathology review

Postrenal azotemia


0 / 5 complete


0 / 1 complete
High Yield Notes
7 pages

Postrenal azotemia

5 flashcards

USMLE® Step 1 style questions USMLE

1 questions

A 65-year-old man comes to the emergency department for evaluation of lower abdominal discomfort for an hour. He has not urinated since yesterday and has had difficulty initiating urination for the past three months. He has not had weight loss, dysuria, urgency, or dribbling of urine. The patient had a viral illness two days ago for which he started taking acetaminophen for fever. Current vitals are within normal limits. Physical examination demonstrates a palpable mass in the suprapubic area. A symmetric, enlarged non-tender prostate is palpated on digital rectal examination. Glomerular filtration rate is 40 ml/min/1.73m2. Urinalysis is shown.  

 Laboratory value  Result 
 Serum chemistry 
 Blood urea nitrogen  36 mg/dL 
 Creatinine  1.9 mg/dL 
 Proteinuria  Absent 
 Dysmorphic red blood cells  Absent 
 Sodium (UNa 15 mEq/L 
 Fractional excretion of sodium (FENa <1% 
 Urine osmolality  650 mOsm/kg 
 Sediment  None 
If left untreated, which of the following laboratory findings are most likely to be observed in the coming weeks? 

External References

Content Reviewers:

Rishi Desai, MD, MPH


Tanner Marshall, MS

Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function.

AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys.

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff!

Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule. Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion.

Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function!

Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away. Meanwhile, the filtered blood drains into the renal vein.

Alright, so with postrenal AKI, there’s some obstruction to the outflow from the kidneys.

Reduced flow can be a result of something compressing the ureter like intra-abdominal tumors, or compressing the urethra further down, like from benign prostatic hyperplasia—a noncancerous growth of the prostate gland, both of which sort of pinch the ureter or urethra shut.

Also though it could be some blockage inside, like kidney stones getting stuck in the ureter or urethra, which actually plug it up. Now, if only one ureter’s obstructed, called unilateral obstruction, and the other kidney’s working fine, then renal function’s usually preserved. If, say, both ureters are obstructed, called bilateral obstruction, or the urethra gets blocked, then we’ve got a recipe for postrenal AKI.

Whatever the obstruction is, it ultimately causes this buildup of urine and pressure that backs up into the kidney; all the way to the millions of tiny renal tubules.


Postrenal azotemia is a condition characterized by an excessive level of nitrogen-containing waste products in the bloodstream (azotemia) due to obstruction of the urinary tract. Postrenal azotemia can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Postrenal azotemia can lead to kidney failure if left untreated. Treatment typically involves medical or surgical interventions to remove the obstruction.

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Acute kidney injury" The Lancet (2019)
  6. "Management of severe hyperkalemia" Critical Care Medicine (2008)
  7. "Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group" Critical Care (2004)