716,935views
00:00 / 00:00
Renal system
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
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
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
Prerenal azotemia
0 / 50 complete
0 / 2 complete
of complete
of complete
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 |
2022
2021
2020
2019
2018
2017
2016
renal failure p. 627
renal failure p. 626
renal failure p. 627
renal failure consequences p. 626
renal failure and p. 627
renal failure and p. 627
renal failure p. 627
in renal failure p. 627
with renal failure p. 627
renal failure causing p. 626
renal failure p. 627
renal failure p. 626
renal failure p. 627
renal failure p. 627
renal failure p. 627
renal failure p. 627
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
renal failure p. 627
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.
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.
Copyright © 2023 Elsevier, except certain content provided by third parties
Cookies are used by this site.
USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.