AKI Flashcards
AKI due to scleroderma (scleroderma renal crisis) should be treated with
ACE inhibitors.
for hepatorenal syndrome:
Bridge therapies that have shown promise include terlipressin (a vasopressin analog), combination therapy with octreotide (a somatostatin analog) and midodrine (an a1-adrenergic agonist), and norepinephrine, in combination with what intravenous fluid?
albumin (25–50 g, maximum 100 g/d)
Idiopathic TTP-HUS is a medical emergency and should be treated promptly with
plasma exchange
Early and aggressive volume repletion is mandatory in patients with rhabdomyolysis, who may initially require
10 L of fluid per day
Alkaline fluids may be beneficial in preventing tubular injury and cast formation, but carry the risk of worsening _______.
- 75 mmol/L sodium bicarbonate added to 0.45% saline
* hypocalcemia
According to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines, patients with AKI should achieve a total energy intake of
20–30 kcal/kg per day
Protein intake should vary depending on the severity of AKI: 0.8–1.0 g/kg per day in noncatabolic AKI without the need for dialysis; 1.0–1.5 g/kg per day in patients on dialysis; and up to a maximum of ______ if hypercatabolic and receiving continuous renal replacement therapy.
1.7 g/kg per day
a technology similar to hemodialysis except at lower blood flow and dialysate flow rates.
CRRT Continuous renal replacement therapy can also be performed by diffusive clearance (continuous venovenous hemodialysis [CVVHD]
in which large volumes of plasma water (and accompanying solutes) are forced across the semipermeable membrane by means of hydrostatic pressure;
Continuous renal replacement therapy (CRRT) can be performed by convective clearance (continuous venovenous hemofiltration [CVVH]
A hybrid therapy combines both diffusive and convective clearance
continuous venovenous hemodiafiltration [CVVHDF]
To achieve some of the advantages of CRRT without the need for 24-h staffing of the procedure, some physicians favor _____ or extended daily dialysis (EDD).
In this therapy, blood flow and dialysate flow are higher than in CVVHD, but the treatment time is reduced to ≤12 h.
slow low-efficiency dialysis (SLED)
If available, is often preferred in patients with severe hemodynamic instability, cerebral edema, or significant volume overload.
CRRT
Continuous renal replacement therapy
Common causes of community-acquired AKI include
volume depletion heart failure adverse effects of medications obstruction of the urinary tract malignancy
The most common clinical settings for hospital-acquire AKI are
sepsis
major surgical procedures
critical illness involving Heart or liver failure
nephrotoxic medication administration
is the most common form of AKI. It is the designation for a rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration
Prerenal azotemia
Prolonged periods of prerenal azotemia May lead to ischemic injury, often termed
acute tubular necrosis (ATN)
Glomerular filtration can be maintained despite reduced renal bloodflow by _____, which-maintains glomerular capillary hydrostatic pressure closer to normal and thereby prevents marked reductions in GFR if renal blood flow reduction is not excessive
angiotensin II–mediated renal efferent vasoconstriction
Intrarenal biosynthesis of vasodilators such as____
increase in response to low renal Perfusion pressure
prostaglandins(prostacyclin, prostaglandin E2), kallikrein and kinins,and possibly nitric oxide (NO)
Even in healthy adults, renal autoregulation usually fails once the systolic blood pressure falls below
80 mmHg
can also occur following percutaneous catheterization of the aorta, or spontaneously, is due to cholesterol crystal embolizationresulting in partial or total occlusion of multiple small arteries withinthe kidney.
AKI from atheroembolic disease
Individuals undergoing massive fluid resuscitation for trauma, burns, and acute pancreatitis can also develop _______, where markedly elevated intraabdominal pressures, usually >20 mmHg, lead to renal vein compression and reduced GFR
the abdominal compartment syndrome
The most common clinical course of contrast nephropathy is characterized by a rise in SCr beginning ___ following exposure, peaking within 3–5 days, and resolving within 1 week
24–48 h
1-2days (nor exceeding 2 days and after 1 day post exposure)
transient tubule obstruction with precipitated contrast material agents implicated as a cause of AKI are
- high-dose gadolinium used for magnetic resonance imaging (MRI) and
- oral sodium Phosphate solutions used as bowel purgatives.
- Iodinated contrast agents use din CV CT SCANS
Antibiotics that cause AKI
Vancomycin
Aminoglycosides and amphotericin B
Acyclovir
Clinical features of amphotericin B nephrotoxicity include
polyuria,
hypomagnesemia
hypocalcemia,
non-gap metabolic acidosis.
Antibiotic that can precipitate in tubules and cause AKI by tubular “obstructions” particularly when given as an intravenous bolus at high doses (500 mg/m2) or in the setting of hypovolemia.
Acyclovir
are also frequently associated withAKI due to tubular toxicity
Acyclovir Foscarnet pentamidine tenofovir cidofovir
may Cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria, hypokalemia,and a modest decline in GFR.
Ifosfamide
Chemotherapeutic agents casing AKI
Ifosfamide
Cisplatin and carboplatin
bevacizumab
Toxic Ingestions causing AKI
Ethylene glycol
HEAA
Diethylene glycol
Aristolochic acid
the most common protein in urine and produced in the thick ascending limb of the loop of Henle
uromodulin
may follow initiation of cytotoxic therapy in patients with high-grade lymphomas and acute lymphoblastic leukemia; massive release of uric acid (with serum levels often exceeding15 mg/dL) leads to precipitation of uric acid in the renal tubules and AKI (Other features include hyperkalemia and hyperphosphatemia
Tumor lysis syndrome
contamination of foodstuffs has led to nephrolithiasis and AKI, eitherthrough intratubular obstruction or possibly direct tubular toxicit
Melamine
distinctions-of ckd to AKI ,clues suggestive of CKD can come from
radiologic studies (small,shrunken kidneys with cortical thinning on renal ultrasound, or evidence of renal osteodystrophy)
or
laboratory tests such as normocytic anemia in the absence of blood loss or secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
Prerenal azotemia should be suspected in the setting of
vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.
Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes
Recent manipulation of the aorta or other large vessels; may occur spontaneously or after anticoagulation;retinal plaques, palpable purpura,livedo reticularis, GI bleed
Labs: Hypocomplementemia, eosinophiluria(variable), variable amounts ofproteinuria
Atheroembolic disease
Complete anuria early in the course of AKI is uncommon except in thefollowing situations:
complete urinary tract obstruction, renal artery Occlusion, overwhelming septic shock, severe ischemia (often with cortical necrosis), or severe proliferative glomerulonephritis or vasculitis
In CKD, kidneys are usually smaller unless the patient has
diabetic nephropathy,
HIV-associated nephropathy,
or infiltrative diseases.
In cases-of oliguric AKI, the urinary flow rate in response to bolus intravenous furosemide 1.0–1.5 mg/kg can be used a prognostic test: urine outputof less than ____ after intravenous furosemide may identify patients at higher risk of progression to more severe AKI, and the need for renal replacement therapy.
200 mL over 2 h
The definitive treatment of the hepatorenal syndrome is
orthotopic liver transplantation
AKI due to scleroderma(scleroderma renal crisis) should be treated with
ACE inhibitors
Early and aggressive volume repletion is mandatory in patients withrhabdomyolysis, who may initially require
10 L of fluid per day
Alkaline diuretics
Alkaline fluids (e.g., 75 mmol/L sodium bicarbonate added to 0.45% saline
Diuretics may be used if fluid repletion is adequate but unsuccessful in achieving urinary flow rates of 200–300 mL/h.
Management of Tumor lysis syndrome:
aggressive intravenous fluids and allopurinol or rasburicase
Management for Volume overload
Salt and water restriction
Diuretics
Ultrafiltration
In severe cases of volume overload, furosemide may be given as a bolus
(200 mg) followed by an intravenous drip (10–40 mg/h), with or without a thiazide diuretic
Hyperphosphatemia is commonin AKI and can usually be treated by limiting intestinal absorption of phosphate using phosphate binders:
calcium carbonate calcium acetate lanthanum sevelamer or aluminum hydroxide
According to the Kidney Disease Improving Global Outcomes(KDIGO) guidelines, patients with AKI should achieve a total energy intake of
20–30 kcal/kg per day
According to the Kidney Disease Improving Global Outcomes(KDIGO) guidelines, patients with AKI should achieve a total protein intake of
1.7 g/kg per day if hypercatabolic and Receiving continuous renal replacement therapy
