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Year 3 Renal & Urology > Renal failure > Flashcards

Renal failure Flashcards

1
Q

What is AKI?

A

Acute kidney dysfunction resulting in acute renal failure: impairment of renal function over days/weeks which results in raised urea/creatinine and oliguria (fall in urine output). It is usually reversible.

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2
Q

What is the aetiology of AKI? (x3 (x2, x8 and x4)

A
  • PRE-RENAL (decreased renal perfusion): shock (hypovolaemia, sepsis, cardiogenic (hypotension)), hepatorenal syndrome (liver failure)
  • RENAL (aka INTRINSIC): acute tubular necrosis, acute glomerulonephritis, acute interstitial nephritis, small/large vessel obstruction, light-chain nephropathy, urate nephropathy, pigment nephropathy, accelerated phase hypertension e.g., pre-eclampsia
  • POST-RENAL: stone, tumour (pelvic, prostate, bladder), blood clots, retroperitoneal fibrosis
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3
Q

What is the aetiology of acute tubular necrosis? (x3) What is it?

A

Damage of tubular epithelial cells caused by ischaemia, drugs and toxins (paracetamol, AMINOGLYCOSIDES (antibiotics), NSAIDs, ACEi and lithium).

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4
Q

What is the aetiology of acute interstitial nephritis? (x4) What is it?

A

Inflammation of renal tubulo-interstitium caused by NSAIDs, penicillin, sulphonamides and leptospirosis (Leptospira bacterial infection of the blood).

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5
Q

What is the aetiology of small/large vessel obstruction? (x4)

A

Renal artery/vein thrombosis, cholesterol emboli, vasculitis, HUS/TTP (haemolytic microangiopathy).

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6
Q

What is the aetiology of light-chain nephropathy? What is it?

A

The kidney is a site of metabolism of Ig light chain proteins – reabsorbed in the proximal tubule and catabolised by intracellular lysosomal enzymes. Damage to proximal tubular cells or increased production of light chains means these light chains appear in the urine and deposit in the proximal tubule. This is caused by myeloma.

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7
Q

What is the aetiology of urate nephropathy? What is it?

A

Deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. This is caused by lympho- or myeloproliferative disorders, particularly after chemotherapy induced cell lysis.

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8
Q

What is the aetiology of pigment nephropathy? (x2) What is it?

A

Pigment nephropathy is an abrupt decline in renal function as a consequence of the toxic action of endogenous heam-containing pigment in the kidney. Such pigments include myoglobin, released from skeletal muscle in rhabdomyolysis, and haemoglobin, released during intravascular haemolysis.

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9
Q

What is rhabdomyolysis?

A

Condition when damaged skeletal muscles breaks down (typical in elderly falls with long period of lying), leading to myoglobin release which may cause AKI.

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10
Q

What is the pathophysiology of pre-renal AKI? (x3)

A

In response to hypoperfusion, there is activation of renin-angiotensin-aldosterone system (Ang II vasoconstricts; aldosterone promotes water and sodium reabsorption at collecting duct) and increased SNS stimulation (increased baroreceptor firing from reduced BP leads SNS-mediated constriction of efferent arteriole and dilation of afferent). There is also raised ADH release leading to tubular water retention.

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11
Q

What is the pathophysiology of acute tubular necrosis AKI?

A

Impaired kidney perfusion and tissue hypoxaemia leads to ischaemia and microvascular endothelial injury, most severe in the proximal tubule and outer-medullary segments. This can be pre-disposed by damage and toxin-mediated vasoconstriction.

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12
Q

What is the pathophysiology of post-renal AKI?

A

Obstruction leads to increased intratubular pressure resulting in tubular ischaemia and atrophy. In chronic forms of obstruction, there is also monocyte/macrophage recruitment and cytokine-mediated irreversible tubular injury.

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13
Q

What is the epidemiology of AKI: Most common cause?

A

Most common cause is ATN (acute tubular necrosis).

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14
Q

What are the signs and symptoms of AKI? (x6)

A
  • Mainly symptoms of CAUSE or COMPLICATIONS
  • Hypotension
  • Oliguria
  • Oedema
  • N&V (may cause pre-renal AKI or may be a complication of AKI-related uraemia)
  • Haematuria
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15
Q

What are the blood investigations for AKI? (x5)

A
  • METABOLIC PROFILE: high urea and creatinine. LFTs to assess for hepatorenal syndrome. Creatinine kinase is high in rhabdomyolysis
  • VBG: hyperkalaemia, hyponatraemia (hypernatremia in pre-renal), low bicarbonate, and metabolic acidosis.
  • FBC: high/low WBC to assess for sepsis cause, platelets to assess for HUS/TTP, anaemia for HUS/myeloma/vasculitis
  • CRP: high if infective aetiology
  • BLOOD CULTURE: sepsis
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16
Q

What are the other investigations for AKI? (x6)

A
  • FLUID CHALLENGE: good response to a fluid challenge supports a diagnosis of pre-kidney AKI.
  • URINE: proteinuria/haematuria and culture and sensitivity
  • CXR: monitor for fluid overload (pulmonary oedema)
  • ECG: check for hyperkalaemia
  • RENAL USS: exclude obstructive cause
  • RENAL BIOPSY: for certain aetiologies e.g., acute tubular nephritis: tubulitis and interstitial cellular infiltrate including eosinophils
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17
Q

What are the signs of renal AKI in urinalysis?

A

Decreased renal osmolality/specific gravity and raised urine sodium from decreased renal concentrating ability, increased fractional excretion of Na+ (PCr.UNa/PNa.UCr)

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18
Q

What are the signs of pre-renal AKI in urinalysis?

A

Increased renal osmolality/specific gravity and decreased urine sodium from raised renal concentrating ability, decreased fractional excretion of Na+ (PCr.UNa/PNa.UCr)

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19
Q

How is AKI diagnosed?

A

Acute rise in creatinine (within 48 hours or 1.5 times baseline in last 7 days) and/or sustained reduction in urine output.

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20
Q

What is the caveat of measuring creatinine to diagnose AKI?

A

Has 24-hour delay from kidney injury.

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21
Q

What are the complications of AKI? (x5 +5)

A

Hyperkalaemia, sepsis, metabolic acidosis (decreased bicarbonate), pulmonary oedema, hypertension. LESS COMMON: Uraemia (can lead to pericarditis and encephalopathy), gastric ulceration, bleeding (from platelet dysfunction), muscle wasting (hypercatabolic state), acute cortical necrosis.

22
Q

How is AKI managed generally?

A
  • Treat complications: hyperkalaemia, metabolic acidosis, pulmonary oedema
  • Treat cause
  • Hemofiltration/dialysis
23
Q

How is AKI managed: hyperkalaemia? (x5)

A
  • 10mL calcium gluconate IV (protects heart against arrythmias; remember, calcium is part of depolarisation)
  • 50mL 50% dextrose with 5U act-rapid insulin over 15 minutes (drive potassium into cells)
  • Nebulised salbutamol can also reduce potassium
  • Ca2+/Na+ resonium PO/PR (decrease bowel absorption) e.g., calcium-polystyrene sulfonate
  • Dialysis if appropriate
24
Q

How is AKI managed: metabolic acidosis?

A

50-100mL of 8.4% bicarbonate via central line over 15-30 mins.

25
Q

How is AKI managed: pulmonary oedema? (x4)

A
  • O2, consider CPAP
  • IV GTN 2-10 mg/h (vasodilator, reduce BP)
  • IV furosemide (loop diuretic): 250mg over 1 hour, followed by infusion (5-10 mg/h)
  • IV diamorphine (single dose of 2.5mg) relieves anxiety and breathlessness
26
Q

What may be the cause of oedema in AKI? (x2)

A

Aggressive fluid resuscitation in pre-renal AKI or oliguria

27
Q

How is AKI managed: treating the cause? (x3 +1)

A
  • STOP AKI: Sepsis, Toxins, Optimise BP/volume, Prevent harm (treat complications)
  • SEPSIS
  • Review medications: stop nephrotoxins
  • FLUID RESUSCITATION: 500mL bolus of crystalloid 0.9% saline over 15 mins. Reassess using ABCDE and give additional boluses if needed. Consider vasopressor such as noradrenaline/vasopressin also
    • RELIEVE OBSTRUCTION: urinary catheter is urinary outflow obstruction, stent if ureter obstruction
28
Q

What are the indications for hemofiltration/dialysis in AKI? (x5)

A
  • Persistent hyperkalaemia (K+ over 7mmol/L)
  • Fluid overload such as refractory pulmonary oedema
  • Pericarditis
  • Acidosis (arterial pH less than 7.1, bicarbonate less than 12 mmol/L)
  • Symptomatic uraemia (tremor, cognitive impairment, coma, fits, urea typically above 45 mmol/L)
29
Q

What is the difference between hemofiltration and dialysis?

A

Both are forms of RENAL REPLACEMENT THERAPY. HEMOFILTRATION: CONTINUOUS arteriovenous/venous-venous filtration of plasma water across membrane induced by the hydrostatic pressure gradient, and ‘convective’ transport of solutes in the same direction as water. Substitution fluid is required to prevent excessive fluid removal. DIALYSIS: INTERMITTENT haemodialysis (using central venous catheters/AV fistulae) or peritoneal dialysis. Solutes passively diffuse down their concentration gradient.

30
Q

How do you choose between hemofiltration and dialysis?

A

Hemofiltration preferred in hypotensive or haemodynamically unstable patients since the rate of fluid and solute removal is slow. Dialysis preferred in haemodynamically stable.

31
Q

How do you treat pigment nephropathy? (x2)

A

Maintain diuresis with saline, carefully monitoring for fluid overload, to wash out pigment. Switch to alkaline solution (bicarbonate) once diuretic has been established, since raised urine pH (above 6.5) may release free iron from myoglobin deposited in tubules. Add a loop diuretic/mannitol if diuresis cannot be established.

32
Q

How do you treat urate nephropathy? (x3)

A

Allopurinol, loop diuretic and fluids to wash out the obstructing uric acid crystals.

33
Q

What is the prognosis of AKI?

A

In-patient mortality of 20%. Usually reversible.

34
Q

What is chronic kidney disease? Defined as? (x2)

A

AKA chronic renal failure. Defined as kidney damage or GFR below 60ml/min/1.73m^2 for 3 months. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.

35
Q

How is CKD staged? (x5)

A
  1. GFR over 90
  2. 60-89
  3. 30-59
  4. 15-29
  5. Less than 15
36
Q

What is the aetiology of CKD? (x4 (x3, x4, x3 and x3) +5)

A
  • VASCULAR: hypertension (cause and consequence), renal artery atheroma, vasculitis
  • GLOMERULAR DISEASE: glomerulonephritis, diabetes, amyloidosis, SLE
  • TUBULOINTERSTITIAL DISEASE: pyelonephritis/interstitial nephritis, nephrocalcinosis, TB
  • CONGENITAL/INHERITED: polycystic kidney disease, Alport’s syndrome, congenital hypoplasia
  • Myeloma
  • HIV nephropathy
  • Scleroderma
  • Gout
  • Obstructive uropathy: renal tumour or enlarged prostate
37
Q

What is glomerulonephritis?

A

Spectrum disorder characterised by inflammation of the glomerulus

38
Q

What is pyelonephritis?

A

Upper urinary tract infection affecting renal pelvis and calyces, typically caused by bacterial infection from lower UTI.

39
Q

What is interstitial nephritis?

A

AKA tubulointerstitial nephritis. Inflammation of renal interstitium caused commonly by infection of drugs.

40
Q

What is nephrocalcinosis?

A

Excess calcium deposition in the kidneys.

41
Q

What is Alport’s syndrome?

A

Genetic disorder characterised by glomerulonephritis and hearing loss, associated with mutations in type IV collagen synthesis.

42
Q

What is scleroderma?

A

Autoimmune condition of increased collagen synthesis leading to sclerosis (stiffening of tissue), damage to microvasculature and activation of T lymphocytes.

43
Q

What are risk factors for CKD? (x2)

A

Family history and climate (heat stress nephropathy)

44
Q

What is the pathophysiology of CKD? (x4)

A
  • Regardless of aetiology, the same cascade happens following damage:
  • In response to injury, there is increase in intra-glomerular pressure and glomerular hypertrophy as the kidney adapts to nephron loss
  • There is subsequent increase in glomerular permeability to macro-molecules such as TGF-beta, fatty acids and protein which may result in mesangial cell expansion, (participate in regulation of filtration rate), inflammation and glomerular scarring
  • Renal injury results in an increase in Ang-II causing upregulation of TGF-beta and further scarring and subsequent functional loss
  • There is also tubule-interstitial disease associated with infiltration of WBCs
45
Q

What is the epidemiology of CKD: Most common cause? Where? Ethnicity?

A

Most common causes are diabetes mellitus followed by hypertension. More prevalent in hotter countries. High prevalence in Black and Hispanic ethnicities.

46
Q

What are the signs and symptoms of CKD? (x6)

A
  • Fatigue (secondary to anaemia/uraemia)
  • Oedema (secondary to fall in glomerular filtration rate and compensatory salt/water retention)
  • N&V, anorexia and pruritus (from accumulation of toxic waste in circulation; urea deposition under skin in pruritus)
  • Restless legs (symptom of uraemia)
  • Kussmaul’s breathing (acidosis)
  • HANDS: leukonychia, brown line at distal end of nail
47
Q

What does foamy urine indicate?

A

Proteinuria

48
Q

Why may patients with CKD get anaemia?

A

Affect production of erythropoietin which drives haemopoiesis.

49
Q

What are the investigations for CKD? (x5)

A
  • BLOOD: elevated serum creatinine, electrolyte abnormalities differ depending on aetiology. Adaptation in acid excretion means there is decreased bicarbonate. Reduced eGFR: can be determined from creatinine and adjusted for age (MDRD calculator).
  • URINALYSIS: haematuria/proteinuria, raised albumin
  • RENAL USS: diagnoses obstruction and stones
  • RENAL BIOPSY: for aetiology
  • AXR/MRI: may reveal stones, renal masses, cysts, lesions (suggestive of aetiology)
50
Q

How is CKD diagnosed?

A

Reduction in GFR for more than 3 months (less than 60 mL/minute/1.73min^2). OR, presence of one or more of the following markers of kidney damage: proteinuria, haematuria, electrolyte abnormalities from tubular disorders, histological abnormalities, structural abnormalities detected by imaging, history of kidney transplantation.

51
Q

How do you differentiate between AKI and CKD? (x4 and x2)

A

DIFFICULT if no repeat creatinine values. The following features favour CKD over AKI: hypocalcaemia, hyperphosphatemia, anaemia, small kidneys on USS. On the other hand, acutely unwell or hypovolaemia favours AKI.

Year 3 Renal & Urology (10 decks)

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