Prerenal azotemia

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Prerenal azotemia

Renal system

Renal and ureteral disorders

Renal agenesis

Horseshoe kidney

Potter sequence

Hyperphosphatemia

Hypophosphatemia

Hypernatremia

Hyponatremia

Hypermagnesemia

Hypomagnesemia

Hyperkalemia

Hypokalemia

Hypercalcemia

Hypocalcemia

Renal tubular acidosis

Minimal change disease

Diabetic nephropathy

Focal segmental glomerulosclerosis (NORD)

Amyloidosis

Membranous nephropathy

Lupus nephritis

Membranoproliferative glomerulonephritis

Poststreptococcal glomerulonephritis

Goodpasture syndrome

Rapidly progressive glomerulonephritis

IgA nephropathy (NORD)

Lupus nephritis

Alport syndrome

Kidney stones

Hydronephrosis

Acute pyelonephritis

Chronic pyelonephritis

Prerenal azotemia

Renal azotemia

Acute tubular necrosis

Postrenal azotemia

Renal papillary necrosis

Renal cortical necrosis

Chronic kidney disease

Polycystic kidney disease

Multicystic dysplastic kidney

Medullary cystic kidney disease

Medullary sponge kidney

Renal artery stenosis

Renal cell carcinoma

Angiomyolipoma

Nephroblastoma (Wilms tumor)

WAGR syndrome

Beckwith-Wiedemann syndrome

Bladder and urethral disorders

Posterior urethral valves

Hypospadias and epispadias

Vesicoureteral reflux

Bladder exstrophy

Urinary incontinence

Neurogenic bladder

Lower urinary tract infection

Transitional cell carcinoma

Non-urothelial bladder cancers

Renal system pathology review

Congenital renal disorders: Pathology review

Renal tubular defects: Pathology review

Renal tubular acidosis: Pathology review

Acid-base disturbances: Pathology review

Electrolyte disturbances: Pathology review

Renal failure: Pathology review

Nephrotic syndromes: Pathology review

Nephritic syndromes: Pathology review

Urinary incontinence: Pathology review

Urinary tract infections: Pathology review

Kidney stones: Pathology review

Renal and urinary tract masses: Pathology review

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Prerenal azotemia

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Prerenal azotemia

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A 40-year-old man presents to the emergency department with difficulty breathing over the past two days. His past medical history is significant for chronic liver disease secondary to chronic alcohol use disorder. His temperature is 36.6°C (97.8° F), pulse is 80/min, respirations are 21/min, and blood pressure is 125/80 mm Hg. Physical examination shows abdominal distention with shifting dullness. Serum creatinine concentration is 1.5 mg/dL, and serum urea nitrogen concentration is 20 mg/dL. The patient is started on furosemide, and his condition quickly improves. Three days later, repeated laboratory studies show the following:

 Laboratory value  Result 
 Serum 
 Sodium  132 mEq/L 
 Potassium  4.2 mEq/L 
 Chloride  95 mEq/L 
 Creatinine  1.9 mg/dL 
 Albumin  3.2 g/dL 
 BUN/Cr  > 20 
 Urine 
 Erythrocytes  0/hpf 
 Leukocytes  2/hpf 
 Fractional excretion of sodium (FENa <1% 
 Urine osmolality  600 mOsm/kg 
 Sediment  None 
 
 Which of the following is the most likely explanation for these laboratory findings? 

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Anemia

renal failure p. 627

Anorexia (symptom)

renal failure p. 626

Asterixis p. 80, 537

renal failure p. 627

BUN (blood urea nitrogen)

renal failure consequences p. 626

Developmental delay

renal failure and p. 627

Dyslipidemia

renal failure and p. 627

Encephalopathy

renal failure p. 627

Erythropoietin p. NaN

in renal failure p. 627

Growth retardation

with renal failure p. 627

Heart failure p. 318

renal failure causing p. 626

Hyperkalemia p. 614

renal failure p. 627

Hypertension p. 306

renal failure p. 626

Intrinsic renal failure p. 626

Metabolic acidosis p. 616

renal failure p. 627

Nausea

renal failure p. 627

Pericarditis

renal failure p. 627

Pulmonary edema

renal failure p. 627

Renal failure

diabetes mellitus p. 352

enterotoxigenic Escherichia coli (EHEC) p. 143

Fabry disease p. 86

guanosine analogs p. 198

labs/findings p. 723

myoclonus in p. 537

preeclampsia and p. 667

prolactin elimination in p. 336

tetracyclline use in p. 189

Uremia

renal failure p. 627

Transcript

Content Reviewers

Rishi Desai, MD, MPH

Contributors

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 prerenal kidney injury is due to a decreased blood flow into the kidneys.

So if you’ve got your body fluid, with fluid in circulating in the plasma as well as all the other intracellular and extracellular fluid. So a decreased blood flow could be due to an absolute loss of body fluid, where fluid actually leaves the body.

Summary

Prerenal azotemia is a form of azotemia in which the kidneys fail to adequately filter waste products from the blood, due to reduced renal perfusion. This can be caused by dehydration, excessive blood loss, heart failure, or any condition that decreases blood flow to the kidneys. Treatment of prerenal azotemia focuses on addressing the underlying cause, such as increasing fluid intake or treating the underlying condition.

Elsevier

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