Acute Kidney Injury and ESRD Flashcards
Prerenal Azotemia
Causes
Increased BUN and creatinine with BUN rising more than creatinine
- Hypotension (systolic below 90 mmHg) from sepsis, anaphylaxis, bleeding and dehydration
- Hypovolemia: diuretics, burns and pancreatitis
- Renal artery stenosis
- Relative hypovolemia from decreased pump function: CHF, constrictive pericarditits and tamponade
- Hypoalbuminemia
- Cirrhosis
- Hepatorenal syndrome
- Abdominal compartment syndrome
- NSAIDs (constricts afferent arteriole)
- ACEIs and ARBs (dilate efferent arteriole)
Postrenal Azotemia
Causes
- Prostate hypertrophy or cancer
- Stone in the ureter
- Cervical cancer
- Urethral stricture
- Neurogenic (atonic) bladder
- Retroperitoneal fibrosis (bleomycin, methylsergide or radiation)
Azotemia due to intrinsic renal disease
Causes
- Acute tubular necrosis (ATN)
- Ischemia or toxins
- Acute glomerulonephritis like RPGN or hemolytic uremic syndrome
- Acute (allergic) interstitial nephritis
- Crystals such as hyperuricemia, hypercalcemia or hyperoxaluria
- Proteins such as Bence-Jones protein from myeloma
- Thromboembolism
- Atheroembolic disease
Acute Tubular Necrosis (ATN)
Causes
- Ischemic (secondary to decrease in renal blood flow) in which PCT and thick ascending limb are highly susceptible to injury:
- Hypotension
- Sepsis
- CHF
- Nephrotoxic in which PCT is particularly susceptible to injury:
- Aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir and cyclosporine (all with onset of 5-10 days). Also low Mg++ increase the aminoglycosides and cisplatin toxicity
- Contrast media (immediate renal toxicity). Can be prevented with saline hydration. also sodium bicarbonate and N-acetylcysteine can be used but with no consistent proven benefits
- Hemoglobinuria and myoglobinuria (rhabdomyolysis)
- Hyperuricemia from tumor lysis syndrome (acute) or gout (chronic renal failure)
- Calcium oxalate precipitation in renal cortex from ethylene glycol overdose
- Bence-Jones protein (directly toxic to renal tubules)
- NSAIDs
Acute (allergic) Interstitial nephritis (AIN)
Causes
- Most common is due to drugs that act as haptens, inducing hypersensitivity reactions (drug allergy and rash, Stevens-Johnson syndrome, Toxic epidermal necrolysis, and Hemolysis):
- Penicillins and cephalosporins
- Sulfa drugs including diuretics
- Proton pump inhibitors
- NSAIDs
- Phenytoin
- Rifampin
- Quinolones
- Allopurinol
- Rarely due to:
- Systemic infection like mycoplasma
- Autoimmune disease like SLE, Sjogren syndrome and sarcoidosis
Drugs that are extremely rare to be associated with AIN or hypersensitivity reactions
- Calcium channel blockers
- Beta-blockers
- SSRIs
Renal Papillary Necrosis
Causes
- Sickle cell disease or trait
- NSAIDs
- DM
- Acute or chronic pyelonephritis
- Urinary obstruction
Prerenal Azotemia
Diagnosis
- BUN:creatinine is > 20:1
- Urine Na+ is < 20 mEq/L
- Fractional excretion of Na+ (FENa) is < 1%
- Urine osmolality is > 500 mOsm/kg (high specific gravity)
Intrinsic Renal Disease
Diagnosis
- BUN:creatinine is < 20:1
- Urine Na+ is > 20 mEq/L
- Fractional excretion of Na+ (FENa) is > 1%
- Urine osmolality is < 300 mOsm/kg (low specific gravity)
Note: The exception to this rule is ATN due to contrast media (can cause ATN within few days) where: - BUN:creatinine is < 20:1
- Urine Na+ is < 10 mEq/L
- Fractional excretion of Na+ (FENa) is < 1%
- Urine osmolality is > 500 mOsm/kg (high specific gravity)
Tumor Lysis Syndrome
Prevention
All of these should be given prior to chemotherapy:
- Allopurinol
- Hydration
- Rasburicase
Rabdomyolysis
Causes
- Trauma or crush injuries
- Prolonged immobility
- Snake bites
- Seizures
Rabdomyolysis
Diagnosis
- Urine analysis (best initial test): +ve dipstick with no cells on microscopic examination
- Elevated Creatinine phosphokinase (CPK)
- Hyperkalemia (release from cells)
- Hyperuricemia (release of nucleic acids that will be metabolized to uric acid [this wont occur in hemolysis because RBCs have no nuclei])
- Hypocalcemia (due to calcium binding to damaged muscles)
Rabdomyolysis
Treatment
- Saline hydration
- Mannitol
- Sodium bicarbonate (drive K+ into cells and may prevent myoglobin precipitation in renal tubules)
Acute Tubular Necrosis (ATN)
Treatment
- No therapy proven to benefit ATN
- Hydration of volume depleted
- Correction of electrolytes
- Diuretics just increase the U.O.P, but do not change overall outcome
Urgent Dialysis
Indications
- Fluid overload
- Uremic complications like encephalopathy, pericarditis and bleeding
- Metabolic acidosis
- Hyperkalemia
- Toxins:
- Salicylates
- Theophylline
- Methanol
- Barbiturates
- Lithium
- Ethylene glycol
Renal Failure Consequences
- Metabolic acidosis
- Hyperkalemia and hypermagnesemia
- Dyslipidemia (increased triglycerides)
- Uremia (nausea and anorexia, pericarditis, encephalopathy, asterixis, and platelet dysfunction)
- Na+ and water retention which leads to HF, pulmonary edema and hypertension
- Growth retardation and developmental delay
- Anemia (erthropoietin failure)
- Renal osteodystrophy, hypocalcemia (D3 deficiency), and hyperphosphatemia (due to high parathyroid hormone levels)
- Infections (defect in degranulation of neutrophils)
- Pruritis
- Accelerated atherosclerosis and hypertension
- Endocrinopathy: anovulation (women), low testosterone and erectile dysfunction (men), increased insulin levels (renally excreted) and increased insulin resistance (glucose level may be up or down)
Hepatorenal Syndrome
Treatment
- Midodrine
- Octreotide
- Albumin
Atheroemboli
Presentation
- Blue/purplish skin lesions in fingers and toes
- Livedo reticularis
- Ocular lesions
Atheroemboli
Diagnosis
- Eosinophilia and eosinophiluria
- Low complement level
- Elevated ESR
Acute (allergic) Interstitial nephritis (AIN)
Diagnosis
- Elevated BUN and creatinine with a ratio < 20:1
- White and red cells in urine
- Eosinophilia and eosinophiluria
Acute (allergic) Interstitial nephritis (AIN)
Treatment
- Usually resolves spontaneously with stopping the drug or controlling the infection
- Severe cases are manged with temporary dialysis
- If creatinine continues to rise after stopping the drug then give glucocorticoids (predinsone, hydrocortisone and methylprednisolone)
Analgesic Nephropathy
Presentation
- ATN
- AIN
- Membranous glomerulonephritis
- Vascular insufficiency of the kidney
- Papillary necrosis
Renal Papillary Necrosis
Presentation
Resembles that of acute pyelonephritis:
- Sudden onset of flank pain
- Fever
- Hematuria
Renal Papillary Necrosis
Diagnosis
- Urine analysis shows white and red cells, and may show necrotic renal tissue
- Urine culture is -ve
- CT scan shows “bumpy” contour of internal renal structures where papillae were lost
End Stage Renal Disease (ESRD)
Causes
- Diabetes
- Hypertension
- Any form of tubular or glomerular damage
End Stage Renal Disease (ESRD) associated Anemia
Treatment
Erythropoietin replacement and iron supplementation
End Stage Renal Disease (ESRD) associated Hypocalcemia and Osteomalcia
(Treatment)
Vitamin D and calcium replacement
End Stage Renal Disease (ESRD) associated Bleeding
Treatment
DDAVP which will increase platelet function (use only when bleeding is present)
End Stage Renal Disease (ESRD) associated Pruritis
Treatment
Dialysis and ultraviolet light
End Stage Renal Disease (ESRD) associated Hyperphosphatemia
Treatment
- Give oral phosphate binders:
- Calcium acetate
- Calcium carbonate
- Sevelamer (only when Ca++ level is high)
- Lanthanum (only when Ca++ level is high)
- Also treat hypocalcemia to decrease the levels of parathyroid hormone
Note: never use Aluminum containing binders because Aluminum causes dementia
End Stage Renal Disease (ESRD) associated Hypermagnesemia
Treatment
Restriction of high magnesium foods, laxatives and antacids
End Stage Renal Disease (ESRD) associated Atherosclerosis
Treatment
Dialysis
End Stage Renal Disease (ESRD) associated Endocrinopathy
Treatment
- Dialysis
- Estrogen and testosterone replacement
Renal Transplantation
Facts
- Only 50% of ESRD patients will be suitable for transplantation
- The donor does not have to be alive or related, although these are both better
- HLA-identical, related donor kidneys last 24 years on average
Diffuse Cortical Necrosis
Pathology
Acute generalized cortical infarction of both kidneys due to a combination of vasospasm and DIC
Diffuse Cortical Necrosis
Causes
- Obstetric catastrophes like abruptio placentae
- Septic shock
Renal Osteodystrophy
Definition and Pathology
- Subperiosteal thinning of bones seen in ESRD
- Hypocalcemia and hyperphosphatemia with vitamin D3 deficiency that will lead to secondary hyperparathyroidism; also hyperphosphatemia will decrease serum Ca++ by causing tissue calcifications, whereas decrease in D3 will decrease intestinal Ca++ absorption