Renal azotemia

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Renal azotemia

Renal system


Renal azotemia


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Renal azotemia

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A 50-year-old man comes to his primary care physician’s office for routine follow-up. He was recently diagnosed with osteoarthritis of the knees four weeks ago and was initiated on analgesic medications. Past medical history is significant for diabetes mellitus. Current medications include metformin, naproxen and acetaminophen. His vitals and physical exam are within normal limits. Laboratory results are as follows.  

 Laboratory value  Results 
  4 weeks ago  Today 
 Serum chemistry 
 Sodium  138 mEq/L  137 mEq/L 
 Potassium  4 mEq/L  4.1 mEq/L 
 Bicarbonate  24 mEq/L  25 mEq/L 
 Chloride  96 mEq/L  94 mEq/L 
 Creatinine  1.1 mg/dL  1.6 mg/dL 
 Protein  100 mg/day  102 mg/day 
 Cast  None  None 
 Blood  negative  negative 
Changes to which of the following anatomic regions is most likely accountable for this patient’s rise in creatinine?  

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Acute interstitial nephritis p. 626


acute interstitial nephritis p. 626


acute interstitial nephritis with p. 626

Furosemide p. 253, 632

interstitial nephritis p. 253


acute interstitial nephritis p. 626

Hematuria p. 620

interstitial nephritis p. 626

Hypersensitivity reactions p. 110-111

acute interstitial nephritis p. 626

Interstitial nephritis

acute p. 626

as drug reaction p. 252

NSAID toxicity p. 499

penicillins p. 185

Mycoplasma spp.

interstitial nephritis with p. 626

Nonsteroidal anti-inflammatory drugs (NSAIDs) p. 499

acute interstitial nephritis p. 626

interstitial nephritis p. 250, 252


interstitial nephritis from p. 626

Proton pump inhibitors (PPIs) p. 407

acute interstitial nephritis p. 626

Rifampin p. 193

acute interstitial nephritis from p. 626

Sarcoidosis p. 701

acute interstitial nephritis p. 626

Sjögren syndrome p. 478

acute interstitial nephritis with p. 626

SLE (systemic lupus erythematosus)

acute interstitial nephritis p. 626

Sulfonamides p. 191

acute interstitial nephritis from p. 626


Content Reviewers

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.

Typically intrarenal AKI’s due to damage to the tubules, the glomerulus, or the interstitium—the space between tubules. Starting with the tubules and the most common cause of intrarenal AKI, which is acute tubular necrosis. Which is where the epithelial cells that line the tubules necrose, or die. One way this can happen is via ischemia, or a lack of blood supply to the cells.


Renal azotemia refers to an elevation of nitrogen-containing waste products in blood like urea and creatinine, which are due to renal dysfunction often causing an acute kidney injury (AKI). AKI is said when the kidneys aren't functioning at 100%, and it has developed relatively quickly, typically over a few days.

AKI can be classified into three main types: intrarenal, prerenal, and postrenal AKI. In intrarenal AKI, kidney injury is caused by something within the kidneys themselves. Examples include conditions like acute tubular necrosis, glomerulonephritis, or acute interstitial nephritis. In prerenal AKI, there is reduced blood flow to the kidneys, and this hypoperfusion results in kidney injury. It's commonly seen following dehydration, or shock (e.g. hypovolemic and septic shocks). In postrenal AKI, a blockage in the urinary tract prevents urine from leaving the kidneys, which impairs normal kidney functioning and damages them. Postrenal AKI can be caused by conditions like bladder stones, prostate enlargement in men, or urinary tract tumors.


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