Nephrology Acute renal failure

Acute Renal Failure

Is a clinical syndrome in which a sudden deterioration in renal function results in inability of the kidney to maintain fluid and electrolyte homeostasis.


The driving force for glomerular filtration is the pressure gradient from the glomerulus to the Bowman space. Glomerular pressure is primarily dependent on renal blood flow (RBF) and is controlled by combined resistances of renal afferent and efferent arterioles. Regardless of the cause of ARF, reductions in RBF represent a common pathologic pathway for decreasing GFR.

CRITERIA

ESTIMATED CCl
URINE OUTPUT
Risk
eCCl decrease by 25%

Injury

eCCl decrease by 50%

Failure

Loss

End-stage

eCCl = estimated creatinine clearance

The etiology of ARF comprises 3 main mechanisms. Prerenal failure Is caused by decrease in the circulating arterial volume, which leads to inadequate renal perfusion & decreased glomerular filtration rate, evidence of kidney damage is absent.


Depressed RBF eventually leads to ischemia and cell death. The initial ischemic insult triggers a cascade of events that includes production of oxygen free radicals, cytokines and enzymes, endothelial activation and leukocyte adhesion, activation of coagulation.


Recovery from ARF is first dependent upon restoration of RBF. In prerenal failure, restoration of circulating blood volume is usually sufficient. Rapid relief of urinary obstruction in postrenal failure results in a prompt decrease of vasoconstriction. With intrinsic renal failure, removal of tubular toxins and initiation of therapy for glomerular diseases decreases renal afferent vasoconstriction.

Common causes of acute renal failure:

Prerenal
Renal
Postrenal
Dehydration Hemorrhage Sepsis Hypoalbuminemia Cardiac failure
GN(PSGN, SLE, ,HSP, membranoproliferative) HUS, Acute tubular necrosis Renal vein thrombosis Rhabdomyolysis Acute interstitial nephritis Tumor infiltration Tumor lysis syndrome
Posterior urethral valve. Ureteropelvic junction obstruction Ureterovesicular junction obstruction Ureterocele Tumor Urolithiasis Hemorrhagic cystitis Neurogenic bladder



History Infants with history of acute GE & dehydration most likely has prerenal RF. 6yr old child with a recent pharyngitis who presented with periorbital edema, hypertension & gross hematuria most likely has intrinsic ARF

Neonate with history of hydronephrosis on prenatal ultrasound & a palpable bladder most likely has congenital urinary tract obstruction like posterior urethral valve. The presence of rash & arthritis may suggest SLE or HSP nephritis. Palpable flank masses may suggest renal vein thrombosis, tumors, cystic disease, or urinary tract obstruction.

Common manifestations of established ARF: Pallor, anorexia, nausea, vomiting. GI bleeding( hematemesis and melena). Fluid overload and pulmonary edema, hence cough, orthopnea and pulmonary rales. Congestive HF, hypertension and pericarditis. Neurologic complications include: headache, fatigue, muscle twitching, confusion, hallucinations. Decreased immunity and liability to infections.

Urinalysis -- Normal urinary sediment without hemoglobin, protein, cells, or casts generally consistent with prerenal and postrenal failure Granular casts == glomerulonephritis, interstitial nephritis RBC casts =Glomerulonephritis WBC casts = Pyelonephritis

Blood urea nitrogen (BUN): is usually elevated but it correlates poorly with the GFR Serum creatinine is increased.


Complete blood cell count: Anemia (dilutional or hemolytic as in SLE, renal vein thrombosis, & HUS, or blood loss, or decreased erythropoiesis). Or leucopenia (SLE), thrombocytopenia( SLE, renal vein thrombosis, HUS). Platelets dysfunction.


Blood biochemistry: Hypocalcemia (moderate) is common in ARF, due to increase phosphate level Hyperkalemia is a common and important complication of ARF. Hyponatremia. Metabolic acidosis Serum C3 level may be depressed (post strep. GN) , & antinuclear Ab(SLE).


Electrocardiography: Obtain routine ECGs to look for manifestations of hyperkalemia and arrhythmias Renal biopsy: is often helpful in finding specific cause of intrinsic renal failure, is especially important when glomerular causes of ARF are suspected.



Urinary indices in distinguishing prerenal from intrinsic ARF:
index
Prerenal
Intrinsic renal
Specific gravity Urine osmolality (mosm) Urine sodium (meq/L) Fractional Excretion of Na Blood urea nitrogen/creatinin

<1.010 <350 >40 >2% <20

Bladder catheter should be placed especially in cases of obstruction & in nonambulatory patient to ensure adequate urine drainage. Determination of volume status is important in the initial evaluation of patients with ARF.


In case of hypovolemia, intravascular volume should be expanded by IV administration of isotonic saline 20ml/kg over 30 min After volume resuscitation, hypovolemic patients generally void within 2hr: failure to do so points toward presence of intrinsic or postrenal ARF.


In general glucose containing solutions 10-30% without electrolytes are used as a maintenance fluids & the fluid is modified according to electrolyte balance. Fluid intake, urine & stool output, body weight, & serum chemistries should be monitored on daily basis.

Metabolic acidosis: Mild acidosis is common as a result of retention of hydrogen ions; phosphate & sulfate, but rarely requires treatment. If acidosis is severe (PH <7.15; serum bicarbonate<8meq/L) should be corrected by IV sodium bicarbonate to raise arterial PH 7.2.


Hypocalcemia: Patient should follow low phosphorus diet & phosphate binders should be given by mouth to bind any ingested phosphate & increase gastrointestinal phosphate excretion, e.g calcium carbonate, the starting dose 1-3 tablets with meal. GI symptoms Oral or IV H2 blockers such as ranitidine can be given.


Neurologic symptoms in ARF may include headache, seizure, lethargy & confusion. Diazepam is the most effective agent in controlling seizure.


Correction of anemia and if Hb falls below 7g/dl, give packed RBC Nutrition is of critical importance, sodium, potassium, & phosphorus should be restricted. Protein intake should be restricted moderately while maximizing caloric intake to minimize accumulation of nitrogenous wastes.

Dialysis: indicated in the following: 1-Volume overload with evidence of hypertension &/or pulmonary edema refractory to diuretic therapy. 2-Persistent hyperkalemia. 3-Severe metabolic acidosis unresponsive to medical management. 4-Neurologic symptoms (altered mental status, seizures)

5-Blood urea nitrogen greater than 100-150 mg/dl or lower if rapidly rising. 6-Calcium/phosphorus imbalance, with hypocalcaemic tetany.

Three types of dialysis available: 1-Intermittent hemodialysis: useful in patients with relatively stable homodynamic status, it can be done 3-7 times a week. 2-peritoneal dialysis: Hyperosmolar dialysate is infused into the peritoneal cavity via a percutaneously placed catheter, the fluid is allowed to dwell for 45-60 min & is then drained from the patient by gravity, cycles are repeated for 8-24 hr/day based on patients fluid & electrolyte balance. It is contraindicated in abdominal disorders.

3--Continuous renal replacement therapy: This is useful in patients with unstable hemodynamic status, concomitant sepsis, or multiorgan failure in the intensive care unit; it is an extracorporeal therapy in which fluid, electrolytes, & small & medium sized solutes are continuously removed from the blood (24hr/day).


The mortality rate in children with ARF depends on the nature of the underlying disease process rather than on the renal failure itself. In general, children with ARF caused by renal limited conditions (postinfectious GN) have a very low mortality rate < 1% Those with ARF related to multiorgan failure have a very high mortality rate >90%.