Most common cause AKI in Outpatient is pre renal : hypotension,vomiting, diarrhea,gastroenteritis
Most common hospital acquired AkI is Acute tubular necrosis bec medication or prolonged pre renal
Two drugs cause AKI
NSAID: vasoconstriction afferent so dec blood flow to renal
ACEI: vasodilation efferent so inc blood flow from renal
Pathophysiology of AKI
Pre-renal (If prolonged will lead to acute tubular necrosis)
Renal
Post-renal (Obstruction at any site from renal tubule to theurethra)
Increased BUN:creatinine ratio
> 20
FENa (%) (fractional excretion of Na)
< 1%
Decreased BUN:creatinine ratio
FENa (%) (fractional excretion of Na) > 2%
Causes of decreased blood flow to kidneys
Stenosis
Obstruction blood flow of kidney
Hemorrhage shock
Hypovolemic shock
Heart failure
Sepsis
Normally function of renal reabsorption of Na and excretion K
Creatinine
Measured function renal self
BUN
Increased by pre-renal bec dehydrate
FENa
Excretion of Na and reabsorption K
Isolated high BUN with normal creatinine is due to Upper GI Bleeding
Increased BUN : Creatinine ratio >20
Due to crush injury, marathone runners
Acute tubular necrosis is the most common cause of hospital acquired AKI
Acute tubular necrosis
Due to drug, toxin or prolonged pre-renal state
Presence of Muddy brown cast or granular cast
Urine Na high
FeNa > 2%
RBCs Cast or dysmorphic red cells indicates glomerulonephritis
Muddy brown or granular cast in ATN
Hyaline cast in pre-renal causes
WBC cast indicates infection or interstitial nephritis
Fatty cast in nephrotic syndrome
Waxy cast in chronic kidney disease
Acute interstitial nephritis
Triad of eosinophilia, fever and rash
Presence of pyuria and eosinophiluria
Eosinophiliuria DDx:- AIN and cholesterol emboli
Rhabdomyolysis causes dark tea color urine with dipstick +ve for blood but no erythrocyte on UA
Rhabdomyolysis follows heat exposure or crush injury
Rhabdomyolysis has High CK level
Treatment of Rhabdomyolysis is IV fluid
Contrast induced nephropathy causes increased serum creatinine within 24 to 48 hours following contrast exposure
High risk for CIN:- recent AKI, eGFR < 30
Only approved prophylaxis for CIN is IV 0.9 saline and use of iso-osmolar or low osmolar contrast
No benefit of N-acetylcystine, dialysis post-contrast or sodium bicarbonate infusion for CIN
Indications for renal replacement therapy
Refractory hyperkalemia
Refractory fluid overload
Refractory acidosis
Uremic pericarditis or uremic encephalopathy
Intoxication
Acute Renal replacement therapy
Replaces nonendocrine kidney function in patients with renal failure. Techniques include intermittent hemodialysis, continuous hemofiltration and hemodialysis, and peritoneal dialysis
Small kidneys on ultrasound suggest chronicity except in DM, HIV, Polycystic kidney disease, Amyloidosis
Most common cause of death in ESRD patient is cardiovascular diseases
Diabetic nephropathy
Protein > 3.5 Gm in diabetic patient, Clinical diagnosis, absence of diabetic retinopathy make it unlikely cause of proteinuria
Screen for diabetic nephropathy with albumin/creatinine ratio annually starting from time of diagnosis for Type 2 DM and 5 years after diagnosis for Type 1 DM
Treatments to delay progression of CKD
BP control
Glycemic control
ACEi in case of proteinuria
SGLT-2 inhibitors (Empagliflozin)
Low protein diet (but not restricted and not in case of nephrotic syndrome)
Sodium bicarbonate only in case of metabolic acidosis
Anemia in chronic kidney disease
Anemia of chronic inflammation, treated with SC Erythropoietin
Iron deficiency anemia should be ruled out first and if present to be treated first
Transferrin saturation < 20% + Ferritin < 100 à Iron supplement