Nephro- Acute & chronic renal failure

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48 Terms

1
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What are the essentials of diagnosis for ARF/AKI?

Sudden inc in BUN or serum Cr, oliguria

2
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What is a condition in which the GFR is abruptly reduced, causing sudden retention of endogenous & exogenous metabolites that are normally cleared by the kidneys?

Acute renal failure (ARF)

3
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How is the urine output usually in ARF?

Low (< 400 ml/d), but can see anuria or high/normal if renal concentrating mechanisms impaired

4
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What is a useful marker for ARF?

Serum Cr (increases in absence of functioning kidneys)

5
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What are the 3 categories of ARF?

Prerenal azotemia, postrenal azotemia, intrinsic renal disease

6
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What is the MCC of ARF & is due to renal hypoperfusion?

Prerenal azotemia

7
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What can happen if hypoperfusion persists in prerenal azotemia?

Ischemia which can cause intrinsic renal failure

8
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What are the 3 ways that decreased renal perfusion can occur, causing prerenal azotemia?

Dec in intravascular volume, change in vascular resistance, low cardiac output

(volume depletion can be caused by hemorrhage, GI loss, dehydration, excessive diuresis, pancreatitis, burns, trauma, peritonitis)

9
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What labs are seen in prerenal azotemia?

Bun/Cr ratio > 20:1

UNA < 20 (low)

FENA < 1 (low)

Urinary sediment: hyaline casts

10
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What is the treatment for prerenal azotemia?

Maintenance of euvolemia, monitor serum K, avoid nephrotoxic drugs

11
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What is the least common cause of ARF & is reversible?

Postrenal azotemia

12
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What category of ARF occurs when urinary flow form both kidneys or single functioning kidney is obstructed, usually a urologic problem?

*each nephron has inc intraluminal pressure → dec GFR

Postrenal azotemia

13
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What are causes of postrenal azotemia?

Urethral obstruction, bladder dysfunction or obstruction, obstruction of other ureters or renal pelvis, benign prostatic hyperplasia (MCC in men), increased risk with anticholinergic drugs, etc

14
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How can postrenal azotemia present?

Anuric or polyuric, lower abd pain, enlarged prostate, distended bladder, mass palpable on pelvic exam, & obstruction can be constant, intermittent, partial or complete

15
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How do labs appear in postrenal azotemia?

BUN:Cr ratio > 20:1

UNA > 20 (high)

FENA > 1 (high)

Urinary sediment: normal or red cells, white cells, crystals

16
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What is the treatment for postrenal azotemia?

Relieve obstruction ASAP, reversible if caught early

17
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What accounts for half of all AKI cases & is considered after other causes have been excluded?

Intrinsic renal disease

18
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What are the sites of injury in intrinsic renal disease?

Tubules, inters tritium, vasculature, glomerular (parenchymal dysfunction)

19
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What are examples of intrinsic renal disease?

Acute tubular necrosis, acute interstitial nephritis, acute GN

20
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What are the essentials of dx for acute tubular necrosis?

Acute renal insufficiency, ischemia or toxic insult, urine sediment w/ pigmented granular casts & renal tubular epithelial cells

21
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How can acute tubular necrosis present?

Generalized swelling, N/V, oliguria, dec LOC, anorexia, muscle weakness, pulm edema

22
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What is AKI due to tubular damage & accounts for 85% cases of intrinsic ARF?

Acute tubular necrosis (ATN)

23
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What are the 2 major causes of ATN?

Ischemia, nephrotoxin exposure (exogenous > endogenous)

24
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How does ischemia cause ATN?

Occurs in settings of prolonged hypotension or hypoxemia- dehydration, shock, sepsis, major surgery, trauma

25
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What are exogenous nephrotoxins that can cause ATN?

Aminoglycosides, vanco, ceph, cyclosporin, cisplatin, heavy metals, radiographic contrast

26
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What are endogenous nephrotoxins that can cause ATN?

Heme containing products (myoglobin, hgb), uric acid, paraproteins (bence jones)

27
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The following labs are associated with what condition?

  • Brown urine

  • Bun:Cr < 20:1

  • UNA > 20

  • FENA > 1

  • active sediment with dirty muddy brown casts

  • renal tubular epithelial cells & casts

  • hyperkalemia, hyperphosphatemia

ATN

28
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What is the treatment for ATN?

Avoid volume overload, use diuretics w/ caution, nutritional support, phosphate binding agents, dialysis if indicated

29
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What are indications for dialysis in ATN treatment?

Life threatening elyte disturbance (hyperkalemia), volume overload unresponsive to diuretics, worsening acidosis, uremic comps (encephalopathy, pericarditis, seizures)

30
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What are the 3 phases of the course of ATN?

Initial injury

Maintenance phase ~ 3 wks of cellular repair & debris removal (oliguric or nonoliguric)

Recovery phase heralded by dialysis

*MCC death is infx

31
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Which has a better outcome, oliguric or nonoliguric maintenance phase of ATN?

Nonoliguric

32
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What are the essentials of dx of CRF/CKI?

Progressive azotemia over mos-yrs, ssx of uremia when nearing end stage, HTN, isosthenuria & broad casts, metabolic acidosis, B/L small kidneys on US

33
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How is CKI / CRF defined?

Renal damage (based on abnormal UA proteinuria or hematuria) OR

Structural abnormalities found on US (small kidneys) OR

GFR < 60 mL/min ≥ 3 mos

34
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What is 70% of late stage CKD due to?

DM or HTN

35
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The following presentation is with what condition?

  • Nonspecific sx develop slowly, pt remains asx until GFR < 10-15 ml/min

  • Fatigue, malaise, weakness, anorexia, N, V, metallic taste, hiccups

  • Neuro- irritability, difficulty concentrating, insomnia, forgetfulness

  • pruritus, menstrual irregularities, loss of libido

  • PE: chronically ill appearing, HTN, easy bruising, uremic fetor (fishy breath), cardiopulmonary/mental status changes

CRF

36
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The following labs are associated with what condition?

  • elevated BUN & Cr

  • Stage 3 w/ GFR < 30 (refer to nephro)

  • Persistent proteinuria

  • UA: broad, waxy cast

  • metabolic acidosis w/ hyperkalemia

  • anemia of chronic dz

  • low vit D - renal osteodystrophy

CRF

37
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How does CKI appear on imaging?

US → small echoogenic kidneys < 10 cm

XR → renal osteodystrophy

38
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What are treatments for CKI?

Early consults to nephro, vascular, gen surg, dietary

Dietary restrictions

RRT → hemodialysis, peritoneal dialysis, transplant

39
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What restrictions should be implemented in CKI patients?

Protein (~40gm/day),

salt & water (2 g/day),

potassium (< 60-70 mEq/d),

phosphorous (< 4.6 mg/dL, binders if GFR <20-30),

magnesium (no mg laxatives/antacids)

40
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When should RRT be started?

Stage 5 GFR < 15 mL/min or serum Cr of 8 mg/dL

*start diabetics early w/ serum Cr 6 mg/dL

41
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When should CKI pts be referred to nephro?

Stage 3 GFR ~ 30ml/min

42
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What are other absolute indications for RRT (dialysis)?

Uremic sx (pericarditis, encephalopathy, coagulopathy), fluid overload unresponsive to diuresis, refractory hyperkalemia > 7, severe metabolic acidosis pH < 7.20, neuro sx (seizures, neuropathy)

43
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What is the MC choice for RRT?

Hemodialysis → A/V fistula or prosthetic graft, expensive, 3x/wk, monitor elytes, pH, & volume status

44
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What complications are seen with hemodialysis (grafts > fistulas)?

Infx (MC s. aureus), thrombosis, aneurysm

45
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What is the MC complication of peritoneal dialysis?

Bacterial peritonitis (MC s. aureus)

46
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What is peritoneal dialysis?

CAPD → MC, pt exchange dialysate 4-6 times/day

CCPD → cycler machine automatically performs exchange at nigh

*peritoneal membrane is the “dialyzer”

47
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What is the average wait for cadaveric transplant?

2-4 yrs

48
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How many ESRD pts are suitable for transplant?

up to 50% (age becoming less of a barrier)