S10C91 - Acute Renal Failure Flashcards

1
Q

Renal Failure: Approach

A

Prerenal – Intrinsic – Postrenal

Prerenal : decreased perfusion

Intrinsic: pathology in the kidney

Postrenal: obstructive

Community-acquired tends to be prerenal
Hospital-acquired tends to be intrinsic (ATN)

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2
Q

GFR

A
  • 120ml/min/1.73m2 in early adulthood

- decreases by 8 every decade after

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3
Q

ATN

A
  • form of intrinsic kidney injury

- decreased renal perfusion causes ischemic injury to the parenchyma

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4
Q

Postrenal failure

A
  • obstruction initially causes a rise in tubular pressure and thus a decreased driving force for filtration, however the pressure equalizes and after that it is vasoconstrictor properties that continue to depress the GFR
  • relief of obstruction decreases the vasoconstriction
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5
Q

ARF - recovery

A
  • once insult to kidney has been removed, whatever remaining surviving nephrons will hypertrophy to try to boost the GFR, how much the GFR recovers depends on how many nephrons remain
  • if not enough nephrons remain, the hyperfiltration results in sclerosis and actual worsening of function
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6
Q

ARF: Sx

A
  • symptoms are a late finding and are caused by the increased uremia
  • n/v, drowsy, fatigue, confusion, coma
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7
Q

Pre-renal: symptoms and causes

A
  • -pre-renal: thirst, orthostatic light-headedness, decreased u/o
  • causes: n/v/d, excessive urination, hemorrhage, fever, excessive sweating (reduced circulating volume)
  • third spacing causes: sepsis, pancreatitis, burns, heaptic failure
  • overdiuresis: CHF
  • decreased fluid intake
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8
Q

Intrinsic renal failure: symptoms and causes

A
  • flank pain and hematuria: crystal-induced nephropathy, nephrolithiasis, papillary necrosis
  • ischemic AKI: cardiac arrest, severe sepsis, hypotension
  • pigment-induced ARF: rhabdomyolysis, hemolysis (recent TFN) (rhabdo from coma, seizures, intoxication, exercise)
  • myalgias, dark urine, edema, malaise, fever think: glomerulonephritis from previous pharyngitis infxn or skin infxn
  • fever, arthralgia, rash: interstitial nephritis
  • acute renal arterial occlusion: flank pain
  • cough, dyspnea, hemoptysis: pulmonary-renal syndrome (good pasture syndrome, wegener granulomatosis)
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9
Q

Post-renal: symptoms and causes:

A
  • previous prostat dz
  • indwelling bladder catheters are a risk
  • anuria
  • alternating oliguria and polyuria are pathognomonic of obsruction
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10
Q

Pre-renal: DDx

A

Hypovolemia:

  • GI: decreased intake, vomiting, diarrhea
  • diuretics
  • third spacing
  • skin loss: fever, burn
  • other: hypoaldosteronsim, salt-losing nephropathy, post-obstructive diuresis

Hypotension:

  • septic vasodilation
  • hemorrhage
  • decreased CO: ischemic/infarct, valvulopathy, cardiomyopathy, tamponade
  • drugs: BB, CCB
  • high-output failure: thyrotoxicosis, thiamine deficiency, paget dz, AV fistula

Renal artery and small vessel dz:

  • ebolism
  • thrombosis: atherosclerosis, vasculitis, SCD
  • dissection
  • drugs: NSAID, ACEi, ARB, cyclosporine, tacrolimus
  • microvascular thrombosis: preeclampsia, HUS, DIC, vasculitis, SCD
  • hypercalcemia
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11
Q

Postrenal ARF: DDx

A
  • malignancy
  • nephrolithiasis
  • reteroperitoneal dz
  • GU surgery
  • indwelling catheters

Infants/Children:

  • urethra and bladder outlet: anatomic malformations (urethral atresia, meatal stenosis, urethral valves in boys)
  • ureter: anatomic malformations: vesicoureteral reflux (females), ureterovesical jxn obstruction, ureterocele, megaureter (prune belly) syndrome, retrocaval ureter
  • retroperitoneal tumor

All ages:

  • trauma
  • blood clot
  • urethra/bladder outlet: phimosis, urethral stricture, neurogenic bladder (DM, SC dz, MS, parkinson’s), stone, meds (anticholinergics, alpha-adrenergic antagonists, opiates)

Adults:

  • urethra/bladder outlet: BPH, obstructed catheters, cancer (prostate, bladder, Cx, colon)
  • ureter: stones, papillary necrosis (SCD, DM, pyelonephritis), tumor (carcinoma of ureter, uterus, prostate, bladder, colon, rectum, retro-peritoneal lymphoma, uterine leiomyomata), retroperitoneal fibrosis (TB, sarcoid, methylsergie, propranolol, idiopathic), stricutre (TB, radiation, schestosomiasis, NSAIDs), miscellaneous (aortic aneurysm, pregnant uterus, IBD, clot, trauma, surgical accident)
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12
Q

Intrinsic renal failure: Ddx

A

Tubular dz:

  • ischemic ATN
  • nephrotoxins: aminoglycosides, contrast, cisplatin, amphotericin B, heme pigments (rhabdo, hemolysis)
  • obstruction: uric acid, calcium oxalate, myeloma light chains, amyloid
  • obstructive meds: sulfonamide, triamterene, acyclovir, indinavir

Interstitial dz:

  • acute interstitial nephritis: drug rxn (NSAID, Abx, diuretics, phenytoin allopurinol, rifampin)
  • infxn: b/l pyelonephritis, legionnaire dz, hantavirus infxn
  • infiltrative dz: sarcoidosis, lyphoma
  • autoimmune dz: SLE
  • toxins: aristolochic acid (used for wt loss)

Glomerular dz:
-rapidly progressive glomerulonephritis: goodpasture syndrome, wegener granulomatosis, HSP, SLE, membranoproliferative glomerulonephritis, postinfectious glomerulonephritis

Small-vessel dz:

  • microvascular thrombosis: preeclampsia, HUS, DIC, thrombotic thrombocytopenic purpura, vasculitis (polyarteritis nodosa, SCD, atheroembolism)
  • malignant HTN
  • scleroderma
  • renal vein thrombosis
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13
Q

Creatinine

A
  • a pt with a low baseline Cr can lose 1/2 of their functioning nephrons before the develop an elevated Cr level
  • Cr is a breakdown product of muscle protein creatine, therefore the level is linked to muscle mass
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14
Q

urinalysis

A
  • RBC enter filtrate in glomerulonephritis and form casts
  • in ATN, tubular epithelium breaks down and allows pretein to leak into the filtrate and tubular epithelial cells in the sediment
  • hyaline casts are commin in prerenal failure
  • pigmented granular casts are common in ischemic or toxic tubular injury
  • brown granular casts are common in pigment nephropathy (myoglobinuria/hemoglobinuria)
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15
Q

Imaging in ARF

A
  • osbtruction below bladder should be investigate with u/s
  • renal u/s has 90% sensitivity and specificity for identifying hydronephrosis d/t mechanical obstruction
  • noncontrast CT has same sensitivity for hydronephrosis as u/s and can identify the sit and cause of obstruction
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16
Q

Post-obstructive diuresis

A
  • occurs after prolonged obstruction causing renal failure or significant volume overload
  • can lead to significant volume loss and even death
  • admit if pt has persistent diuresis of >250cc/h for >2h with otherwise uncomplicated urethral obstruction
17
Q

Contrast-Induced Nephropathy

A

-becomes an issue once GFR

18
Q

Indications for emergent dialysis:

A
  • uncontrolled hyperkalemia (K>6.5)
  • intractible fluid overload in association with persistent hypoxia, lack of response to conservative measures
  • uremic pericarditis
  • progressive uremic/metabolic encephalopathy, asterixis, Sz
  • serum sodium level 165
  • severe metabolic acidosis resistant to sodium bicarbonate
  • life-threatening poisoning iwth dialyzable drug (lithium, ASA, methanol, ethylene glylcol, theophylline)
  • bleeding dyscrasia secondary to uremia
  • excessive BUN and creatinine levels (should be kept