ACUTE RENAL FAILUREالدكتور خلدون ذنون- كلية طب نينوى- المرحلة الرابعة
Pay attention to the following:
1. Types of ARF.
2. Reversible causes of ARF.
3. Clinical features and laboratory diagnosis of ARF.
4. Essential management steps of ARF.
5. Types of renal dialysis.
6. Indications of renal dialysis.
7. Prognosis of ARF.
DefinitionSudden & usually reversible loss of renal function, developing over days or weeks, plasma creatinine(200(mol/L, oliguria occurs but not always.
CausesPre-renal: heart failure, blood or fluid loss, renal artery stenosis or
occlusion. 2. Intrinsic renal diseases:
Acute tubular necrosis ATN 85%(ischaemic, toxic, septic)
Tubulo-interstitial diseases 10%
Glomerular diseases 5%(primary or part of systemic disease.
3. Post renal: stones, inflammation, tumors.
Causes of rapid loss of renal functionUrinary tract obstruction.
Vascular events: major vascular occlusion, ACEI drugs & RAS, malignant HTN, HUS, TTP.
Rapidly progressive glomerulonephritis e.g vasculitis, SLE.
Acute interstitial nephritis.
Drugs e.g NSAID, ACEI drugs (haemodynamic) penicillins (interstitial nephritis), and aminoglycosides (tubular toxicity).
Reversible pre- renal ARFPathogenesis:(perfusion pressure e.g hypovolaemia, shock, heart failure, renal artery narrowing(dilatation of resistance vessels (prostaglandins(vasodilatation which is impaired by NSAID).If autoregulation of blood flow fails, GFR can still be maintained by constriction of efferent arterioles through renin&angiotensin II which is inhibited by ACEI. If severe & prolonged (blood flow & GFR decline, renal tubules become hyperfunctional i.e (water &Na absorption( urine volume of high osmolality & low sodium.
Diagnosis of pre-renal failureHistory&clinical examination.
progressive(in b.urea & plasma cr., (K, (CO2, (Ca,(PO4.
Urine osmolality(600mosm/kg ; urine Na<20mmol/L ; urine/plasma urea (10:1
Clinical featuresHypotension, poor peripheral perfusion, B.p may be normal, postural hypotension ≥20/10 in hypovolaemia.
Concealed blood loss in: GIT, trauma with fracture femur& pelvis, pregnant uterus.
Large volumes of intravascular fluid lost in to tissues e.g crush injuries, burns, severe inflammatory skin disease, sepsis.
ARF in septic patient: multifactorial i.e bacterial endotoxin , activated mediators. Systemic vasodilation(kidney hypoperfusion (early vasoconstrictors e.g noradrenaline will often restore kidney function). Severe&prolonged sepsis( established ARF with ATN. Sepsis & NSAID is potent cause of ARF.
ManagementTreat underlying cause.
Restore blood volume rapidly e.g blood, plasma, isotonic saline. Monitor CVP or pulmonary wedge pressure.
Isotonic sodium bicarbonate 500 ml 1.26% in severe metabolic acidosis.
Trials do not support use of dopamine in severely ill patient.
In cardiogenic & septic shock: invasive haemodynamic monitoring of cardiac output & systemic vascular resistance. Inotropic drugs are used to restore effective B.P.
Prognosis Early treatment will restore normal renal function; in some cases ARF becomes established.
If severe & prolonged pre-renal failure persist(ATN.
Intrinsic renal disease: rapidly progressive GN, UT obstruction , vasculitis, accelerated hypertension, DIC, allergic interstitial nephritis e.g drugs.
Acute tubular necrosis ATN Ischaemic, nephrotoxic (chemical, bacterial toxins). Pathogenesis
Hypotension & shock( ischaemic tubular necrosis.
(Vasoconstrictors (thromboxane, vasopressin, noradrenaline, angiotensin II ( ( blood flow ( hypoxia of tubular cells which are highly metabolically active ( swelling of cells, impaired mitochondrial function( anaerobic glycolysis & intracellular acidosis, protein & DNA denaturation ( tubular cell death.
Shedding of cells in to tubular lumen ( tubular obstruction.
Oliguric phase, renal blood flow is 20% of normal even when systemic circulation is restored due to endothelial cell swelling of glomeruli & peritubular capillaries with oedema of interstitium.
In nephrotoxic ATN similar changes occur e.g aminoglycosides, cisplatin, amphotericin B.
Tubular cells can regenerate & reform the basement membrane & kidney function returns.
Diuretic phase for several days before returning to normal, due to loss of medullary concentration gradient. Not all patients have diuretic phase.
Clinical features of established ARF( Underlying cause e.g trauma, sepsis +features of renal failure.
( Oliguria <500ml/day,anuria: rare usually due to acute UT
obstruction or vascular occlusion. 20% urine volume normal
or((non-oliguric ARF). ( Rate of rise in urea&cr. depend on rate of catabolism, in severe
infections, major surgery or trauma daily rise in plasma urea
>5mmol/L. ( Disturbance of water, electrolyte & acid base balance.
Hyperkalaemia: common, dilutional hyponatraemia (i.v dextrose,
drink) .Metabolic acidosis, (Ca due to (renal 1,25 DHC. ( Anorexia, nausea, vomiting, later( drowsiness,apathy,
confusion, muscle twiching, hiccough, fits & coma. ( Respiratory rate(due to acidosis, pulmonary oedema or
respiratory infection. ( Pulmonary oedema may result from excess fluids & due
to(pulmonary capillary permeability.
( Anaemia is common due to(blood loss, haemodialysis,
( Bleeding: disordered platelet function, disturbance of coagulation,
GIT bleeding may occur later.
( Infection: depressed humoral & cellular immunity.
InvestigationsUrea, creatinine, electrolytes, calcium and phosphate, serum albumin, full blood count and clotting screen, urine analysis, urine microscopy, renal U/S, culture of urine and blood, chest X-ray, serology for HIV and viral hepatitis before dialysis, ECG.
ManagementHyperkalaemia: >6mmol/L treatment is urgent to prevent cardiac arrythmias.i.v calcium gluconate (protect the heart) & i.v dextrose water with insulin or i.v bicarbonate ( both shifts K+ intracellularly) or haemodialysis.
Restore blood volume by blood, plasma or 0.09% saline depending on (cvp, pwp).
Pulmonary oedema needs dialysis.
U/S to exclude UT obstruction& renal biopsy might be needed to establish the cause of ARF & choice of treatment.
Treatment of underlying conditions:
Corticosteroids & immunosuppressives for vasculitis &RPGN. Steroid may be needed for tubulointerstitial nephritis.
B.P control in accelerated hypertension.
Plasma infusion & plasma exchange in microangiopathic diseases.
Pelvic & ureteric dilatation if found do percutaneous nephrostomy & anterograde pyelography to localize obstruction relieve it urgently.
Fluid & electrolyte balance.Daily fluid intake= urine output + 500ml insensible fluid loss which is higher in fever & tropical areas.Restrict Na&K intake; in diarrhea additional fluid&electrolytes are given, weigh patient daily, avoid dehydration & oedema.
Protein & energy intake: 40 gm protein/day without dialysis.Fat&CHO are given to avoid protein catabolism ; 70gm protein is given with dialysis, some need naso gastric tube feeding. Parenteral nutrition is given in case of vomiting & dirrhoea, bowel is not intact or hypercatabolic state.
Protect patient from infection.
Care with drug use & avoid nephrotoxic drugs.
Renal replacement therapy(dialysis) is indicated in:
Urea(3ommol/L = 180mg/dl S.creatinine(600(mol/L=6.8mg/dl
Hyperkalaemia > 6mmol/L.
Fluid overload if fluid restriction & diuretics fail.
Types of dialysisHaemodialysis, high volume-haemofiltration, continous AV or venovenous haemofiltration, and peritoneal dialysis.
Recovery from ARFUrine volume & blood biochemistry will return to normal. Some with ATN & after relief of UT obstruction a diuretic phase occurs which needs fluid & electrolyte balance, after few days urine volume returns to normal.
PrognosisDepend on underlying disorder & complications
If ARF due to simple bleeding or drugs mortality is low.
ARF with serious infection & multiple organ failure mortality is 50-70%.