1. Renal failure can be acute or chronic, with acute renal failure resulting in the rapid loss of kidney function over hours or days, while chronic renal failure develops over a longer period of time.
2. Acute renal failure is often caused by pre-renal issues like low blood flow due to fluid loss or blood loss, or intrinsic renal disease, and can be diagnosed by reduced urine output, rising creatinine and urea levels, and electrolyte imbalances.
3. Management of acute renal failure focuses on fluid resuscitation to restore blood flow, monitoring for complications, and potentially initiating dialysis for severe cases. Prognosis depends on the underlying cause and presence of multi-organ
1. Renal failure can be acute or chronic, with acute renal failure resulting in the rapid loss of kidney function over hours or days, while chronic renal failure develops over a longer period of time.
2. Acute renal failure is often caused by pre-renal issues like low blood flow due to fluid loss or blood loss, or intrinsic renal disease, and can be diagnosed by reduced urine output, rising creatinine and urea levels, and electrolyte imbalances.
3. Management of acute renal failure focuses on fluid resuscitation to restore blood flow, monitoring for complications, and potentially initiating dialysis for severe cases. Prognosis depends on the underlying cause and presence of multi-organ
1. Renal failure can be acute or chronic, with acute renal failure resulting in the rapid loss of kidney function over hours or days, while chronic renal failure develops over a longer period of time.
2. Acute renal failure is often caused by pre-renal issues like low blood flow due to fluid loss or blood loss, or intrinsic renal disease, and can be diagnosed by reduced urine output, rising creatinine and urea levels, and electrolyte imbalances.
3. Management of acute renal failure focuses on fluid resuscitation to restore blood flow, monitoring for complications, and potentially initiating dialysis for severe cases. Prognosis depends on the underlying cause and presence of multi-organ
1. Renal failure can be acute or chronic, with acute renal failure resulting in the rapid loss of kidney function over hours or days, while chronic renal failure develops over a longer period of time.
2. Acute renal failure is often caused by pre-renal issues like low blood flow due to fluid loss or blood loss, or intrinsic renal disease, and can be diagnosed by reduced urine output, rising creatinine and urea levels, and electrolyte imbalances.
3. Management of acute renal failure focuses on fluid resuscitation to restore blood flow, monitoring for complications, and potentially initiating dialysis for severe cases. Prognosis depends on the underlying cause and presence of multi-organ
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RENAL FAILURE
Dr Uzma Bano FCPS Medicine • ACUTE RENAL FAILURE
vs.
• CHRNIC RENAL FAILURE
Acute renal failure. Loss of renal function in hours or days.
•Is the kidney functioning?
•What caused it to fail? •Can we restore renal function? When does renal failure occur? • Always in the setting of an acute illness not of renal origin. • In patients with multi organ failure. • In the setting of shock from bleeding: accidents, surgery, obstetrical emergencies. • Hypovolemia: gastroenteritis, sweating, loss of fluid into body compartments like paralyzed gut. How do we know the kidney is functioning? . A. Quantity of urine. 1. Normal. 500-> 1.5 litres. 2. OLIGURIA: less than normal. <400ml in 24 hours, <20 ml/hour. Less than 100ml/24 hours is ANURIA. 3. POLYURIA: more than normal >4-6 litres in the absence of intake or signs of dehydration if fluid is restricted. Is the kidney functioning? . Quality of urine. • Concentrating power. Specific gravity or osmolality. Fixed at <1010 or failure to rise in the presence of dehydration and low serum sodium. • Abnormal sediment. • Na concentrating power. • Ratio of urinary creatinine to plasma creatinine. • pH of urine vis a vis pH of blood. Biochemical parameters of renal function. • Blood or serum urea. • Serum creatinine level. • Serum Na, K levels. • pH, HCO³ of blood. • Glomerular filtration rate. 1. Creatinine clearance: 2. Cr EDTA GFR. • Plasma osmolality. 2xNa+2xK+urea+sugar in mmols. Rationale of biochemistry of blood. • Excretion of waste products of metabolism: urea, creatinine, uric acid. • Regulation of electrolytes: sodium, potassium, magnesium. • Excretion of [H]: pH of blood. • Conservation of HCO3: acidosis. • Excretion solutes: plasma osmolarity. What has caused renal failure? • Low renal blood flow: hypovolemia caused by loss of fluid from the vascular compartment or loss of blood. PRERENAL FAILURE. • Disease of renal tissue: acute glomerulonephritis, acute pyelonephritis. INTRINSIC RENAL FAILURE. • Obstruction to urine flow: both ureters obstructed or POST-RENAL FAILURE. Clinical features of Acute Renal Failure • Anorexia, Nausea & vomiting. • Drowsiness, apathy and confusion. • Muscle twitching, hiccoughs • Fits and Coma • All these are late features. The ARF should be detected early by looking for: • Reduced urinary output < 20 ml/hour. • High BUN or doubling of baseline serum creatinine. Clinical setting of acute renal failure.1 Case A. A 40 year old man had a road traffic accident. He fractured his right femur, had a deep cut on the upper arm and injuries to his abdomen. Reached a hospital 6 hours later. He was conscious but disoriented, BP was 80/40, extremities were cold and clammy. X ray confirmed # femur, broken ribs, a hemothorax. On ultra-sound of abdomen the spleen was ruptured. His Hb was 6 gm/dl. He was given IV saline, 3 units of blood, and rushed to surgery. Splenectomy was done, a litre of blood-stained fluid was removed from his abdomen, a chest tube was put in the chest and 600ml of blood was aspirated, his femur was splinted and arm wound was stitched.4 hours post-op he had passed only 20 ml of urine. Initial S creatinine was 1.1 mg/dl & 12 hours later the creatinine was 2.2 mg/dl. Diagnosis : 1. Multiple injuries, blood loss: thigh, abdomen, thorax, arm. 2. Hypovolemic Shock causing low renal perfusion. 3. Acute renal shut down: low urine output, doubling of creatinine. Clinical setting of acute renal failure. 2 Case 2. A 6 year old girl developed diarrhea and vomiting and was brought to the hospital after 2 days. The mother had stopped giving her water and liquids because of the vomiting. Profuse diarrhea persisted. On arrival her eyes were sunken, tongue dry, eyeballs flaccid and she was crying without tears. Her hands and feet were cold and clammy and breathing was deep and sighing. Her BP was not recordable. The mother had not noticed if she had passed urine as there was watery stool. The bladder was empty. She produce no urine out put after IV fluids given to bring her CVP to 6cm of water. Biochemistry. Hb was 12 gm/dl. Ph of blood was 7.1, HCO³ was 16 mmol/l, Serum Na was 129 meq/l, serum K 2.6 meq/l, blood urea was 32 mmol/l, serum creatinine was 4.5 mg/dl. • acute gastro-enteritis. • dehydration and hypovolemia and shock. • acute renal failure with anuria and acidosis. Clinical setting of acute renal failure.3 A 60 year old woman with diabetes was found unconscious at home. She was not taking her medication, had passed large amounts of urine, and had become drowsy. In the hospital she was grossly dehydrated, had an empty bladder and a BP of 90/60 though she was known to be hypertensive. Her blood sugar was 408 mg/dl and ketone bodies were present in her blood and bladder urine. Her urine output after IV fluids was 10 ml/hour. Her blood urea was 120mg/dl, and s. creatinine was 3.4mg/dl. Diagnosis: diabetic keto-acidosis, dehydration, shock and acute renal failure. Clinical setting of Hypovolemia. • Acute gastro-enteritis. • Septicemic shock • Profuse sweating. • Cardiogenic shock, • Uncontrolled diabetes from MI, heart block, • Tachyarrhythmia Intestinal obstruction • • Anaphylactic shock Paralytic ileus • • Acute drug reactions Fluid loss from gastric aspiration. • Transfusion reactions • Burns. • Low serum sodium • Acute pancreatitis. • Low or high serum K Blood loss and low volume. • External injury • DIC. Disseminated • Peri-operative intravascular • Postoperative. coagulation, • Ruptured hollow viscus. • Acute hemolysis. • Ruptured solid organ. • Myoglobinuria. • Antepartum hge. • Complement • Postpartum hge. activation as in • Hge into a body hemodialysis, bypass compartment. surgery • Crush injuries. Evidence of fluid retention. • Breathlessness. • Frothy sputum with cough. • Falling O² saturation. • Crackles at the lung base, bronchospasm. • Peripheral edema. • Enlarging liver. • Batwing edema on the X ray chest. Management of early renal shutdown. • Replace volume: normal saline, plasma, blood, plasma expanders. • Renal dose of dopamine: 2mcg/ml/hour. • Frusamide in large boluses or IV infusion. • Monitor biochemistry. • Monitor urine output. • Check ABGs, pH, HCO³. • Consider dialysis. Management of imbalances. • ACIDOSIS: Patient’s HCO³ × .3 × base deficit= required HCO³. Give 2/3 amount of IV HCO3. Body will correct the rest. • OSMOLARITY. 2Na×2K×urea × glucose. • HYPERKALEMIA: Monitor ECG: tall T waves, absent P, wide QRS complexes, Ventricular fibrillation. • Measure serum SODIUM. Indications for emergency hemodialysis or peritoneal dialysis.. • Failure to improve renal functions with conservative management. • 10 mmol rise in urea/day. • Serum creatinine >6mg/dl. • HCO³ < 10mmol/l. • Serum K >6meq/l. • Pulmonary edema. • Pericarditis, encephalopathy, uremic GI hemorrhage. Prognosis in ARF. • With early fluid replacement 80% will recover. • In severe bilateral cortical necrosis of kidneys and multi organ failure no recovery is possible. • In burns, extensive injury, sepsis, DIC mortality is > 40%. Chronic Renal Failure The National Kidney Foundation - Kidney Disease Outcomes Quality Initiative (NKF-K/DOQI) workgroup has defined CKD as • The presence of markers of kidney damage for > or =3 months, as defined by structural or functional abnormalities of the kidney with or without decreased glomerular filtration rate (GFR), manifest by either pathological abnormalities or other markers of kidney damage, including abnormalities in the composition of blood or urine, or abnormalities in imaging tests
OR
• The presence of GFR <60 mL/min/1.73 m2 for > or =3
months, with or without other signs of kidney damage as described above. CKD Stages • Stage 1 disease is defined by a normal GFR (greater than 90 mL/min per 1.73 m2) and persistent albuminuria
• Stage 2 disease is a GFR between 60 to 89 mL/min per
1.73 m2 and persistent albuminuria
• Stage 3 disease is a GFR between 30 and 59 mL/min per
1.73 m2
• Stage 4 disease is a GFR between 15 and 29 mL/min per
1.73 m2
• Stage 5 disease is a GFR of less than 15 mL/min per 1.73
m2 or end-stage renal disease Relative frequency • • DM • HTN • Glomerulonephritis • Acute tubular necrosis – 45 percent • • Prerenal – 21 percent • • Acute on chronic renal failure – 13 percent • • Urinary tract obstruction – 10 percent • • Glomerulonephritis or vasculitis – 4 percent • • Acute interstitial nephritis – 2 percent • • Atheroemboli – 1 percent Clinical Features • Anorexia, nausea, vomiting, pericarditis, peripheral neuropathy, and central nervous system abnormalities ( lethargy, seizures, coma, and death). • Decreased or no urine output, flank pain, edema, hypertension, or discolored urine. • Asymptomatic elevations in urea, abnormalities on urinalysis. • Systemic symptoms and findings, such as fever, arthralgias, and pulmonary lesions. • Incidental findings (e.g., renal cyst or mass) on radiographic testing performed for some other reason. GFR Estimation Cockcroft-Gault equation Creatinine Clearance= (140-age)×weight in kg 72 ×S Creatinine in mg/dL
For example 68 yr old diabetic weighing 50 kg with
a plasma creatinine of 5 mg/dL (140-68) × 50 = 10 ml/min 72 × 5 Blood tests • Blood CP- anemia of normochromic normocytic type • Electrolytes- Hypo/hypernatremia, hyperkalemia, low bicarbonate, low calcium, high phosphate, metabolic acidosis • Autoantibody screening • Urine analysis RADIOLOGIC STUDIES • Plain film of the abdomen • Ultrasonography • Intravenous pyelogram • CT scan • Magnetic resonance imaging • Renal arteriography • Renal venography • Radionuclide scans • Voiding cystourethrogram • Retrograde or anterograde pyelography Indications for renal replacement therapy • Pericarditis • Fluid overload or pulmonary edema refractory to diuretics • Accelerated hypertension • Acidosis pH <7.1 • Hyperkalemia K> 6.0 • Progressive uremic encephalopathy or neuropathy, • Bleeding diathesis attributable to uremia • Persistent nausea and vomiting • Plasma creatinine concentration above 12 mg/dL (1060 µmol/L, urea of 200 mg/dl or GFR of 15 ml/min