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

Acute Renal Failure (ARF)

AcutePrimary Hypertension due to Endocrine adrenal Hypertension Adrenogenital syndrome Oral Contraceptives. Read more ... » renalDiabetic Nephropathy and Renal complications of DM (Diabetes Mellitus). Read more ... » failure due to intratubular crystal precipitation can be seen in a variety of clinicalPrimary Hypertension due to Endocrine adrenal Hypertension Adrenogenital syndrome Oral Contraceptives. Read more ... » settings, the most common being acute uric acid nephropathyDiabetic Nephropathy and Renal complications of DM (Diabetes Mellitus). Read more ... »

Acute renal failure (ARF) is defined as a sudden decrease of normal kidneyDiabetic Nephropathy and Renal complications of DM (Diabetes Mellitus). Read more ... » function that compromises the normal renal regulation of fluid, electrolyte, and acid–base homeostasis.

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:

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 systemPrimary Hypertension due to Endocrine adrenal Hypertension Adrenogenital syndrome Oral Contraceptives. Read more ... ».
  • Activation of renin angiotensin – aldosterone sys­tem .
  • Release of AVP / ADH (arginine vasopressinVasopressin. Read more ... » / 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

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

Clinical features of ARF

 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

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

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

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