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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
Renal azotemia
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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 |
Urinalysis | ||
Protein | 100 mg/day | 102 mg/day |
Cast | None | None |
Blood | negative | negative |
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acute interstitial nephritis p. 626
acute interstitial nephritis with p. 626
interstitial nephritis p. 253
acute interstitial nephritis p. 626
interstitial nephritis p. 626
acute interstitial nephritis p. 626
acute p. 626
as drug reaction p. 252
NSAID toxicity p. 499
penicillins p. 185
interstitial nephritis with p. 626
acute interstitial nephritis p. 626
interstitial nephritis p. 250, 252
interstitial nephritis from p. 626
acute interstitial nephritis p. 626
acute interstitial nephritis from p. 626
acute interstitial nephritis p. 626
acute interstitial nephritis with p. 626
acute interstitial nephritis p. 626
acute interstitial nephritis from p. 626
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.
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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