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nephrology > Acute Kidney Injury and ESRD > Flashcards

Acute Kidney Injury and ESRD Flashcards

1
Q

Prerenal Azotemia

Causes

A

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)
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2
Q

Postrenal Azotemia

Causes

A
  • Prostate hypertrophy or cancer
  • Stone in the ureter
  • Cervical cancer
  • Urethral stricture
  • Neurogenic (atonic) bladder
  • Retroperitoneal fibrosis (bleomycin, methylsergide or radiation)
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3
Q

Azotemia due to intrinsic renal disease

Causes

A
  • 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
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4
Q

Acute Tubular Necrosis (ATN)

Causes

A
  • 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
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5
Q

Acute (allergic) Interstitial nephritis (AIN)

Causes

A
  • 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
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6
Q

Drugs that are extremely rare to be associated with AIN or hypersensitivity reactions

A
  • Calcium channel blockers
  • Beta-blockers
  • SSRIs
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7
Q

Renal Papillary Necrosis

Causes

A
  • Sickle cell disease or trait
  • NSAIDs
  • DM
  • Acute or chronic pyelonephritis
  • Urinary obstruction
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8
Q

Prerenal Azotemia

Diagnosis

A
  • 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)
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9
Q

Intrinsic Renal Disease

Diagnosis

A
  • 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)
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10
Q

Tumor Lysis Syndrome

Prevention

A

All of these should be given prior to chemotherapy:

  • Allopurinol
  • Hydration
  • Rasburicase
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11
Q

Rabdomyolysis

Causes

A
  • Trauma or crush injuries
  • Prolonged immobility
  • Snake bites
  • Seizures
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12
Q

Rabdomyolysis

Diagnosis

A
  • 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)
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13
Q

Rabdomyolysis

Treatment

A
  • Saline hydration
  • Mannitol
  • Sodium bicarbonate (drive K+ into cells and may prevent myoglobin precipitation in renal tubules)
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14
Q

Acute Tubular Necrosis (ATN)

Treatment

A
  • 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
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15
Q

Urgent Dialysis

Indications

A
  • Fluid overload
  • Uremic complications like encephalopathy, pericarditis and bleeding
  • Metabolic acidosis
  • Hyperkalemia
  • Toxins:
  • Salicylates
  • Theophylline
  • Methanol
  • Barbiturates
  • Lithium
  • Ethylene glycol
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16
Q

Renal Failure Consequences

A
  • 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)
17
Q

Hepatorenal Syndrome

Treatment

A
  • Midodrine
  • Octreotide
  • Albumin
18
Q

Atheroemboli

Presentation

A
  • Blue/purplish skin lesions in fingers and toes
  • Livedo reticularis
  • Ocular lesions
19
Q

Atheroemboli

Diagnosis

A
  • Eosinophilia and eosinophiluria
  • Low complement level
  • Elevated ESR
20
Q

Acute (allergic) Interstitial nephritis (AIN)

Diagnosis

A
  • Elevated BUN and creatinine with a ratio < 20:1
  • White and red cells in urine
  • Eosinophilia and eosinophiluria
21
Q

Acute (allergic) Interstitial nephritis (AIN)

Treatment

A
  • 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)
22
Q

Analgesic Nephropathy

Presentation

A
  • ATN
  • AIN
  • Membranous glomerulonephritis
  • Vascular insufficiency of the kidney
  • Papillary necrosis
23
Q

Renal Papillary Necrosis

Presentation

A

Resembles that of acute pyelonephritis:

  • Sudden onset of flank pain
  • Fever
  • Hematuria
24
Q

Renal Papillary Necrosis

Diagnosis

A
  • 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
25
Q

End Stage Renal Disease (ESRD)

Causes

A
  • Diabetes
  • Hypertension
  • Any form of tubular or glomerular damage
26
Q

End Stage Renal Disease (ESRD) associated Anemia

Treatment

A

Erythropoietin replacement and iron supplementation

27
Q

End Stage Renal Disease (ESRD) associated Hypocalcemia and Osteomalcia
(Treatment)

A

Vitamin D and calcium replacement

28
Q

End Stage Renal Disease (ESRD) associated Bleeding

Treatment

A

DDAVP which will increase platelet function (use only when bleeding is present)

29
Q

End Stage Renal Disease (ESRD) associated Pruritis

Treatment

A

Dialysis and ultraviolet light

30
Q

End Stage Renal Disease (ESRD) associated Hyperphosphatemia

Treatment

A
  • 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
31
Q

End Stage Renal Disease (ESRD) associated Hypermagnesemia

Treatment

A

Restriction of high magnesium foods, laxatives and antacids

32
Q

End Stage Renal Disease (ESRD) associated Atherosclerosis

Treatment

A

Dialysis

33
Q

End Stage Renal Disease (ESRD) associated Endocrinopathy

Treatment

A
  • Dialysis

- Estrogen and testosterone replacement

34
Q

Renal Transplantation

Facts

A
  • 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
35
Q

Diffuse Cortical Necrosis

Pathology

A

Acute generalized cortical infarction of both kidneys due to a combination of vasospasm and DIC

36
Q

Diffuse Cortical Necrosis

Causes

A
  • Obstetric catastrophes like abruptio placentae

- Septic shock

37
Q

Renal Osteodystrophy

Definition and Pathology

A
  • 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

nephrology (7 decks)

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