Acute Renal Failure (ARF) Causes Clinical Features TREATMENT of ARF

Acute Renal Failure (ARF)

Acute renal failure due to intratubular crystal precipitation can be seen in a variety of clinical settings, the most common being acute uric acid nephropathy

Acute renal failure (ARF) is defined as a sudden decrease of normal kidney function that compromises the normal renal regulation of fluid, electrolyte, and acid–base homeostasis.

Acute Renal Failure (ARF) 1

Acute Renal Failure (ARF) Causes Clinical Features TREATMENT of ARF

ARF (Acute renal failure) is characterized by :

  • · Decrease in GFR (reversible).
  • · Retention of nitrogenous wastes.
  • · Disturbance of balance of fluid volume, electrolytes and acid-base.
  • Oliguria: Urine output <0.5 mL/kg/h in infants or <500 mL/1.73 m2/d in older children
  • Anuria: Total cessation of urinary output
  • Polyuria: Urine output >2 L/m2/d in infants and children or 3 L/d in adults
  • ·Oliguria – i.e. urine output <400 ml/day.
  • Pre-renal and post-renal failure may be reversible by prompt and appropriate treatment.
  • ARF is usually asymptomatic. It is diagnosed by a recent increase in blood urea and creatinine.
Acute Renal Failure (ARF) 2

Acute Renal Failure (ARF) Causes Clinical Features TREATMENT of ARF

ARF may be of 3 types:

  • 1. Prerenal
  • 2. Renal
  • 3. Post renal.
  • Pre-renal
    • There is renal hypoperfusion. Renal pa­renchyma is normal.
  • Renal –
    • Renal parenchymal disease is present.
  • Post renal
    • There is urinary tract obstruction lead­ing to renal failure.
  • ARF is mostly reversible.

PRERENAL ARF

  • It is reversible by proper perfusion of kidneys so that glomerular ultrafiltration pressure becomes normal. Renal parenchymal tissue is normal.
  • If tissue hypoperfusion persists there is damage of renal parenchyma.
  • Due to hypoperfusion there is :
  • Activation of sympathetic nervous system.
  • Activation of renin angiotensin – aldosterone sys­tem .
  • Release of AVP / ADH (arginine vasopressin / antidiuretic hormone).
  • Norepinephrine, angiotensin II and AVP cause vasoconstriction in non-essential areas, inhibit salt loss through sweat glands, stimulate thirst, promote salt and water retention.
  • Prostaglandin E2and prostacyclin cause dilata­tion of afferent arterioles.
  • Angiotensin II causes preferential constriction of efferent arterioles.
  • Thus glomerular filtration pressure is increased and glomerular filtration rate is increased.
  • All these processes help to counter the renal hypoperfusion.
  • GFR (Glomerular filtration rate) is maintained only if systemic pressure is above 80 mmHg.

Hepatorenal syndrome

  • In advanced cirrhosis and other liver diseases there is severe form of ARF, called hepatorenal syndrome.
  • Mortality is very high.

INTRINSIC RENAL ARF

  • This may be due to :
  • 1. Disease of larger renal vessels
  • 2. Disease of glomeruli
  • 3. Ischemic and nephrotoxic ARF
  • 4. Tubulointerstitial disease.

Common causes of intrinsic ARF

  • · Ischemia (Acute tubular necrosis)
  • · Nephrotoxins.

Acute tubular necrosis

  • Acute tubular necrosis or Ischemic ARF occurs in trauma, haemorrhage, sepsis, volume depletion. It can occur on preexisting renal disease.

POST RENAL ARF

  • Post renal ARF is usually due to obstructive causes and are fully reversible with surgical treatment .

MAJOR CAUSES OF ARF PRERENAL

  • Haemorrhage
  • Burns
  • Dehydration
  • Vomiting and diarrhea
  • Diabetes mellitus (osmotic diuresis)
  •  Pancreatitis Peritonitis
  •  Hypoalbuminemia
  • Low cardiac output Pulmonary hypertension Sepsis
  • Anti hypertensives
  • Norepinephrine Epinephrine
  • Cirrhosis and ascites (Hepatorenal)
  •  ACE inhibitors
  • Multiple meyloma.

Renal Causes of ARF

  • Renal artery obstruction by thrombus, embolism Renal vein thrombosis
  • Glomerulonephritis
  • Vasculitis
  • Thrombotic thrombocytopeniac purpura Toxaemia of pregnancy
  • DIC (Disseminated intravascular coagulation) SLE (Systemic lupus erythematosus) Scleroderma
  • Acute tubular necrosis (Ischemia or hypoperfusi6n)
  • Toxins
  • PPH (Post Partum Haemorrhage) Abruptio placentae
  • Drugs  Cyclosporin
  •  Antibiotics
  • NSAIDs
  • Radiocontrast dye
  • Interstitial nephritis Infections.
  • Calculi Cancer
  • Clot
  •  Stricture Bladder neck obstruction
  • Urethral obstruction.

Pathophysiology

  • ARF is commonly precipitated by an ischemic or nephrotoxic event.
  • Initial vasodilatation is followed by intense vasoconstriction, with blood redistributed from the cortex to the juxtamedullary nephrons
  • Intratubular debris and cast formation develop.
  • Tubular fluid leaks backward across the injured tubular membrane, which, in addition to tubular obstruction, causes further hemodynamic changes.

FEATURES TO DIFFERENTIATE ACUTE AND CHRONIC RENAL FAILURE ARF

  • Recent increase in urea and creatinine.
  • There is history suggestive of the cause of ARF like diarrhoea, vomiting, burns etc.
  • CRF
  • Anaemia Neuropathy
  • Rena I osteodystrophy Small, scarred kidneys
  • Kidney size may be increased or normal in CRF due to :
  • Diabetic nephropathy Amyloidosis
  • Polycystic kidney disease
  • Usually the kidney size is reduced in CRF .

Clinical features of ARF

  • Thirst
  • Orthostatic hypotension
  • Systemic hypotension (BP <90 mmHg) v Tachycardia (Pulse rate >100 Imin)
  • Tachypnoea
  • Raised JVP
  • Dry skin and mucous membrane
  • Reduced sweating
  • History of NSAIDs, ACE-I (ACE inhibitors), ARBs
  • (Angiotensin receptor blockers) v Decreased urine output
  • Decreased body weig ht
  • Hypovolemia
  •  Sepsis
  •  Hlo Radiocontrast dye
  • Flank pain
  • Atheroembolization suggested by Sic nodules, ischemia of fingers, toes
  • Glomerulonephritis suggested by oliguria, edema, hypertension, active urine sediment.

 Interstitial nephritis suggested by

  • Fever,
  • arthralgias,
  • pruritic (that itch) red rash.

Urinary obstruction suggested by

  • Colicky pain
  • Suprapubic and flank pain
  • oFlank pain – loin tropain.

Prostate enlargement suggested by

  • Nocturia
  • Frequency
  • Hesitancy.

URINE

  • Oliguria or Anuria.

Prerenal ARF

  • · Urine is acellular
  • · Inactive sediments or hyaline casts present.

Post renal ARF

  • · Inactive sediment
  • · Hematuria
  • · Pyuria.

Acute tubular necrosis (ATN) i.e. Ischemic ARF, Nephrotoxic ARF

  • · Pigmented, muddy brown granular casts with tubule epithelial cells in urine.
  • · Mild proteinuria « 19/day

Glomerular involvement

  • Tubulointerstitial disease – RBC casts in urine.

Interstitial nephritis

  • · WBC casts in urine.
  • · Nonpigmented granular casts in urine.

Chronic renal disease

  • Broad granufar casts in urine.
  • Eosinophils -in urine – allergic interstitial nephritis. Uric a~id crystal~ in – acute urate nephropathy.

Proteinuria >1g/day suggests gIomerular disease.

Heavy proteinuria> 1 g/day also seen in patients on NSAIDs, ampicillin, rifampicin, interferon alpha.

Bilirubin in urine in hepatorenal syndrome.

Fractional excretion of sodium

  • FE Na < 1 % in prerenal ARF
  • FE Na > 1 % in ischemic, nephrotoxic (tubular disease).

BLOOD

  • Serum creatinine: increases progressively in renal failure and is a very good indicator of renal failure.
  • Hyperkalemia
  • Hyperphosphatemia
  • Hypocalcemia
  • Hyperuricemia
  • Anaemia

ULTRASOUND

  • Ultrasonography is useful for post renal ARF to diag­nose causes like – urinary tract obstruction, pelvicalyceal dilatation, retroperitoneal fibrosis, neo­plasia.

CT, MRI

PLAIN X-RAY ABDOMEN

  • For nephrolithiasis.

PYELOGRAPHY

retrograde, antegrade

  • for lo­calization of site of obstruction.
  • For patency of renal arteries and veins.

MR ANGIOGRAPHY

  • Non-invasive renal vascular study. CONTRAST ANGIOGRAPHY

RENAL BIOPSY

  • For definitive diagnosis.
  • For intrinsic renal ARF e.g. glomerulonephritis, vas­culitis, thrombocytopenic purpura, interstitial nephri­tis.

COMPLICATIONS

  • There is impairment of renal excretion of sodiurtl, potassium and water.
  • · Volume overload
  • · Raised JVP
  • · Hyponatrem ia
  • · Hyperkalemia
  • · Hyperphosphatemia
  • · Hypocakemia
  • · Hypermagnesemia
  • · Metabolic acidosis
  • · Uremia
  • · Weight gain
  • · Basal lung rales
  • · Dependent edema
  • · Pulmonary edema
  • · Cerebral edema
  • · Seizures
  • · Arrhythmias
  • · Metabolic acidosis
  • · Lactic acidosis
  • · Hemolysis
  • · Leucocytosis
  • · GI bleeding and bleeding from other sites
  • · Infections
  • MI
  • Pericarditis Pericat”dial effusion Pulmonary embolism Uremic syndrome.

Causes of Hypocalcemia in ARF

  • Metastatic deposition of calcium phosphate when the serum calcium X phosphate in mgjdl is > 70.
  • Tissue resistance to parathyroid hormone. Decreased 1,25 dihydroxyvitamin D.

Effects of hypocalcemia

  • Muscle cramps Seizures Hallucinations Confusion
  • Prolonged QT.

TREATMENT OF ARF

  • Prevention of pre-renal and post-renal causes Avoid drugs causing ARF
  • Low drug dosage of nephrotoxic drugs Maintain fluid balance
  • Maintain sodium, potassium, phosphate, calcium levels
  • Invasive and noninvasive hemodynamic moni­toring
  • Low dose dopamine
  • Loop diuretics (frusemide, torsemide) Antihyperte~sives like CCB (Calcium channel blockers) and Alpha-blockers
  • Atrial natriuretic peptide
  • Prostaglandins
  • Antioxidants Glucocorticoids Alkylating agents Plasmapharesis
  • Relief of obstruction of urinary tract
  • Oral or IV sodium bicarbonate if arterial pH <7.2 or serum bicarbonate < 15 meq/L
  • Restriction of dietary phosphate
  • Oral aluminum hydroxide
  • Calcium carbonate
  • Vitamin D
  • Restriction of dietary protein 0.6 g/kg/day Carbohydrate 100 g/day
  • Blood transfusion if required
  • Rarely erythropoietin for anemia
  • Antacids
  • PPI (proton pump inhibitor) and H2blockers Anti biotics
  • Dialysis – if hemodynamically unstable peritoneal dialysis is done
  • Hemodialysis – in uremic syndrome, refractory hyperkalemia, acidosis
  • Continuous renal replacement therapy (CRRT) Continuous arteriovenous hemodiafiltration (CAVHD)
  • Continuous venovenous hemodiafiltration (CVVHD).

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