Acute Renal Failure

Niroj Obeyesekere3rd year student notes

Definition

• Clinical syndrome characterised by rapid (over hours to weeks) decline in GFR, perturbation of extracellular fluid volume, electrolyte and acid base homeostasis, and accumulation of nitrogenous waste products from protein catabolism such as urea or creatinine.

RIFLE criteria

Why is it important

• 1. Common 5% of all hospital admissions and 5-30% in ICU admissions complicated by ARF.

• 2. Community acquired ARF does better than hospital acquired.

• 2. Major cause of in-hospital morbidity and mortality.

• 3. But, most cases are reversible.• 4. and, most cases can be prevented.

Diagnosis

• Serial measurement of urea and creatinine, but this has its limitations,

• 1. GFR may need to fall by 50% for Cr to be outside the “normal” level.

• 2. Reduced muscle mass.• 3. Pre-existing chronic renal insufficiency.• 4. Other substance e.g. drugs that interfere

with lab Cr measurements.

Aetiology

• 1. Prerenal – physiological response to hypoperfusion in which integrity of the renal parenchyma is preserved. Less than 48 hrs.

• 2. Renal – diseases of the renal parenchyma• 3. Postrenal – acute obstruction of the urinary

tract.• Prerenal most common. Prerenal and renal in

terms of ATN is a spectrum of hypoperfusion.

Causes of ARF

Causes of prerenal ARF

Pathophysiology of prerenal renal failure1. True intravacular hypovolaemia2. Decreased effceyive circulatory

volume3. Intrarenal vasoconstriction4. Renal artery disease and

borderline hypovolaemia

Pathophysiology

• Kidney function is maintained by – afferent arteriole vasodilatation by local myenteric reflex, increased PGs, kallikerin and kinins and preferential efferent arteriole constriction by angII.

• Afferent arteriole dilatation is maximal at mean BP of 80. Lesser degrees of hypotension can ARF in HT, DM and elderly.

• Very high Ang II causes both afferent and efferent constriction. Esp with pts with marked circulatory failure.

Pathophysiology

• 1. NSAIDS– reduce Pg production• 2. ACE inhibitors and ARBs- intraglomerular

pressure is dependent on efferent vasoconstriction.

• 3. Diuretics• 4. Nephrotoxics

Intrinsic renal failure

• 1. large renal vessels – artheroemboli, thromboemboli, thromobosis or dissection or vasculitis

• 2. microvasculature and glomeruli – GN, scleroderma, HT, TTP, HUS,

• 3. ischamic and nephrotoxic ATN• 4. tubulointerstitium – interstitial nephritis,

infections, infiltrative.

Post Renal

• Obstruction – only 5% of cases

Clinical approach

Clinical approach

• Some basic questions-• 1.Is it acute, acute on chronic or chronic• 2. is there obstruction• 3. evidence of true hypovolaemia• 4. has there been a major vascular occlusion• 5. is there parenchymal disease other than

ATN

Approach

• Usually blood tests but if not, anaemia, PO4, Ca, kidney size can help to differentiate between acute and chronic.

Clinical evaluation of volume status

Investigations• Urine output – relatively unhelpful in OP setting. If IP can

be useful.• Urine microscopy - useful • Hyaline casts or bland urine prerenal or obstruction.

(blood and pyuria in obstruction)• Muddy brown granular casts in ATN (can be absent in 20-

30%)• Dysmorphic red cells GN• Eosinophiluria – interstitial nephritis• Haemogloburia or myogloburia – haemolysis or rhabdo

Investigations

• Proteinuria – less than 1 g in prerenal or ATN• more than 1 g glomerular proteinuria• Pattern of Cr – Cr increases 24 to 48 hrs in renal

ischaemia, radiocontrast, and atheroembolism.• In contrast nephropathy peaks at 3- 5 days and

returns to normal in 5 to 7.• Normally ATN gets better 7 to 14 days post and

artheroembolic usually irreversible.• Gentamicin Cr increases 7 to 10 days.

Other lab findings

• Hyperkalemia - • Hyperphosphatemia• High K disproportionate might indicate

obstruction or type IV rneal tubular acidosis.• Severe anaemia – haemolysis, MM or TTP.• Thrombocytopenia, dysmorphic red cells in

blood film.

isomorphic

dysmorphic

Muddy casts

Urine microoscopy

Ix-Renal US

Other Ix

• CT KUB• Renal biopsy

Complications of ARF

Complications

• 1. Fluid overload• 2.Hyperkalemia – ECG changes • Peaked t waves• Prolongation of PR interval• Widening of QRS• Heart block, VT, VF asytole.

Complications

• 3. acid base balance- wide anon gap metabolic acidosis

• 4. uremia

Management

When you see a patient with ARF always think

Indications for dialysis