Acute renal failure

Definition: Its characterized by rapid deterioration of renal function over period of hours or days. Its usually associated by oliguria or anuria (< 400cm/day) and can be reversible over a period of days or weeks. medical emergency

Etiology of ARF

Etiology

I- Pre-renal causes

II- Renal cause

III- Post-renal causes

Causes of ARF

I- Pre-renal causes

1- Hypovolemic shock: severe prolonged drop in blood pressure depending on previous renal functions.

Hemorrhage

Severe diarrhea (cholera)Severe vomiting (poisoning).Polyuria (DI).Skin loss (burns).

I- Pre-renal causes

2 -Cardiogenic shock e.g myocardial infarction.

3 -Distributive: Sepsis

4 -Renal artery obstruction:

o Thrombosis or embolism e.g myocardial infarction, infective endocarditiso Renal artery stenosis (after contrast injection or ACEI).

5 -Hepato-renal syndrome In liver failure, acute renal failure appears to result from rapidly reversible vasomotor abnormalities within kidney

II- Renal cause

1 -Glomerular lesion: All causes of acute GN is rare cause with bad prognosis.

2 -Interstitial: Acute interstitial nephritis which might beinfective

(acute necrotising papillitis )or allergic (penicillin, NSAID ,cephalosporin )

II- Renal cause3 -Tubular: (Acute tubular necrosis)

which is either:o Ischemic: In all pre-renal causes if prolonged > 6 hrso Toxic:I- Exogenous: Radicontrast.o Aminoglycosides

o Amphotrecin-B

II- Endogenos: Hemoloytic crisis., Rhabdomyolysis,crush syndrome ( myoglobin toxic to tubule)

Multiple myeloma(tumor of plasma cells )

II- Renal cause

4 -Small vessel disease:o Malignant hypertension cause renal spasm

of afferent arteriole . o Hypertensive crisis in scleriod Hemolytic crisis.o Rhabdomyolysis.o Multiple myeloma.o Cholesterol embolism..o Vasculitis: SLE, PAN.

III- Post-renal causes:

Bilateral obstruction: Urethera: Cancer, stone Bladder: Neurogenic bladder, tumor of trigone, bilateral uretenic stones. Ureters: Bilateral stones or retroperitoneal fibrosis

III- Post-renal causes:

Unilateral obstruction if:o Solitary kidney (the other removal

or non functioning)o Reflex sympathetic inhibition

of healthy kidney.o Stone in urtero-vesical junction o (oedema of trigone) obstruction

of other kidney .

: Case

20 year old African American man comes for screening test for sickle cell . He is found to be heterozygous ( trait or AS) for sickle cell. what is the best advice for him?

a. nothing needed untill he has a painful crisis . b. Avoid dehydration . c. Folic acid supplementation . e. pneumococcal vaccination.

Pathophysiology of ARF

I- Pre-renal :Reduction of RBF is compensated by renal autoregulation through:

1- AngII ( VC of efferent arteriole) +PGs

(VD of afferent arteriole ) i.e. ACEI & NSAID may ppt ARF in hypovolemicpatients.

Pathophysiology of ARF

I- Pre-renal : 2 -Activation of aldosterone &

vasopressin in cases of hypovolemia lead to Concentrated urine:o SG > 1020.o Urine osmolarity > 500 mosmol/L.o Na retention.o Na in urine < 20 mmol/L.o Fe Na < 1%.

Pathophysiology of ARF

II- Renal causes (Mostly secondary to ATN):

-In ischemic necrosis : distal tubules are affected with loss of tubular epithelial cells and basement membrane (bad prognosis)

-In toxic necrosis : the glomeruli & proximal tubules are affected with sparing of basement

membrane (good prognosis).

Pathophysiology of ARF

-It passes into three stages:1 -Oliguria occurs 2ry to:

o Obstruction of tubules by necrotic epithelial cells .

o Back leakage from damaged tubules (ineffective GF) .

o Reflex VC of afferent arteriole.o Glomerular contraction (↓ surface area for filtration).

Pathophysiology of ARF

2 -Polyuric phase:o In ischemic ATN recovery of glomeruli occurs 1st (↑GFR but without improvement in distal tubules (↑ urine output with dehydration).

o Intoxic ATN: recovery of distal tubules before glomeruli (improvement inreabsorptive power without change in GFR (water retention).

Pathophysiology of ARF

3 -Recovery phase: Gradual return of kidney function to normal (may take 3-6 m).

N.B.: In ATN the lesion in renal tubules :o Na reabsorption ( Urinary Na > 40 mEq/L + Fe Na > 1%).o Urine is diluted:o SG < 1010.o Osmolarity < 350.

o Creatinine clearance affected more than urea clearance (urea: creatinine ratio < 40:1 ) (BUN: creatinine < 20:1)

Clinical picture of ARF

It passes into 3 stages

A- Oliguric phase

o Urine < 400 cc/day

o Hyperkalemia:. Is the cause of death may cause severe fatal vent. Tach. and VF

o Skeletal muscle: weakness, flaccidity & paralysis.

o Smooth muscle: Constipation up to paralytic ileus.

o Heart: Bradycardia up to asystole.

o Metabolic acidosis ( kussmel’s breathing) (deep rapid breathing)

A- Oliguric phase:

o Hypervolemia: Hypertension, peripheral, pulmonary& cerebral oedema (convulsions & coma),CHF,basal crepitations ,gallop, only puffiness in eyelids not generalized oedema

o Retention of uremic toxins: urinferous odour of mouth

o Anorexia, nusea, vomiting may be only presentation of ARF, hiccough,pruritis,brain oedema due to hyperosmolarity

o pericarditis ( pain and rub ) , pericardial effusion

o acute abdomen if complicated by peptic ulcer (stress ulcer) leading to severe bleeding or peritonitis

o Convulsions and Coma may supervene

o Hyperphosphatemia: Due to ↓ P+ excretion (binds Ca+ &causes metastatic calcification and Hypocalcaemia due to reduced renal production 1,25 dihydroxycholecalciferol

B- Polyuric phase:

In ischemic necrosis: recovery of glomeruli occurs before tubule:

o ↑ GFR without tubular reabsorption o Diuresis with dehydration & hypokalemia

A careful watch on clinical state, salt and water balance, and serum chemistry is required at this stage, particularly if a major diuretic phase develops. Typically, the diuretic phase lasts for only a few days

C- Recovery phase:

With regaining concentration power of kidney , concentrated urine appears.Complete recovery may take 3-6 months

Clinical picture of cause

•Evidence of dehydration & hypovolemia:

•Low BP, rapid pulse, collapsed neck veins, inelastic skin ,sunken eyes.

Pre-renal cause

•There is severe renal colics with acute onset anuria+ hematuria.PR examination may reveal cause of obstruction (e.g. prostatic enlargement).

post-renal cause

•History of nephrotoxic drug intake, sepsis

Renal cause

: Investigations

I- To diagnose ARF:

Biochemical changes:

>↑Urea, creatinine, uric

acid >↓HCO3.

> ↑K+, dilutional hyponatremia.

>↓PCV (dilutional).

>↓Ca++, ↑ P.+

Urine: Oliguria with low fixed

specific gravity

ECG : for hyperkalemia

>Prominent T wave

>Abscent P wave,

prolonged PR >Wide QRS,

asystole

Decrased GFR(estimated

by cratinine clearance),and

coagulation studies

ABG: low PH CBC:anemia

II- To diagnose the cause:

1 -Pre-renalUrine analysis

1 -BUN: creatinine> 40

2 -Urine Na.: < 20 mmol/L

3 -SG.: > 10204 -Urine osmolarity:

> 500 mmol/L

2 -In renal causes:Urine analysis

1 -BUN: creatinine< 402 -Urine Na.: < 20 mmol/L

3 -SG.: < 10104 -Urine osmolarity: < 350

mmol/L5 -Red cell casts (AGN).6 -Epithelial cases (ATN)

(diagnostic).7 -Pus cells (acute

pyolonephritis).8 -Hemoglobinuria

(hemolysis) or myoglobinuria (crush

syndrome).9 -Renal biopsy if the

cause unclear for > 4 weeks.

3- In post renal causes:

1- Abdominal X-ray. Or Abdominal sonar to detect cause of obstruction find back pressure changes and

exclude end stage kidney (shrunken )

2- Ascending pyelography

How to reach the diagnosis:

Treatment:Before persistent oliguria

1 -In pre-renal causes.

•Blood transfusion for hemorrhage•Plasma transfusion for burns. Inotropic

support in case of HF

2 -In post renal causes

• Catheterization.• Suprapubic cystostomy or nephrostomy to relief

•obstruction

Before persistent oliguria:

3 -In renal causes:

•Trial of forced diuresis by:•o Lasix infusion (up to 1 gm).

•o Mannitol 20%: 500 ml IV• infusion.

•o Dopamine (2-5 ug/kg/min).•o Avoid nephrotoxic drugs.

•o Alkalnization of urine in• myoglobinunia ,• hemoglobinuria

A- In oliguric phase:

1 -Treatment of hyperkalemia: ↓Intake: restrict K in diet.

Intracellular shift :o Glucose 25% 100 cc + 20 U regular insulin infusion over 3 hrs.o Na HCO3 100 ml (4.2% solution). Rapid correction of acidosis in a hypocalcaemic patient may also trigger tetany, since hydrogen ions displace calcium from albumin- binding sites, thus increasing physiologically active calcium concentration in blood.o B2 stimulation: Salbutamol IV or inhalation.

↑Excretion:o Resonium A

( Na exchange resin that binds K in GIT) given orally or rectally .

o Dialysis if K > 7 mEq/L.o Antagonize effect on heart :

Ca gluconate 10% solution 10 ml slowly.

2 -Treatment of acidosis:Oral or IV NaHCO3 if HCO3 < 12 meq/L or pH < 7.2.

3 -Treatment of uremia:Restriction of protein in diet (0.5 gm/kg/day).Excess carbohydrate in diet and Vitamin supplements are usually supplied. Vitamin D analogue therapy and pharmacological doses of erythropoietin are not employed routinely.anabolic steroids to avoid endogenous protein catabolism.Dialysis: If urea > 100 mg% or rising > 40 mg% per-day (hypercatabolic).

4 -Correction of fluid overload: > Fluid balance :intake =urine output + insensible water loss

(vapour ,stool, sweat) . > Fluid restriction: Volume of urine/day + 500 cc insensible loss

+500ml/1oC fever. > Large changes in daily weight reflecting change in fluid balance

status should also prompt a reappraisal of the situation > Treatment of acute pulmonary oedema (Dialysis).

> Treatment of convulsions: anticonvulsants + cerebral dehydrating measures.

5 -Correction of hyperphosphatemia : Avoid P+ (in milk) + give AlOH3 or CaCO3 to

P+ absorption.

6 -Dialysis: is indicated if: K > 6.5 mEq/L.

HCO3 < 12 or pH < 7.2. Urea > 100 mg% or ↑ by 40 mg% daily.

Emergency cases e.g. HF or encephalopathy, pericarditis or severe bleeding.B- In diuretic stage : In excess diuresis : Give IV fluids + Na & K supplements.C- In recovery phase: gradual ↑ in protein intake

Comparisons of dialysis modalities

Peritoneal dialysis (PD) is used infrequently in the management

Data suggest that PD is significantly less effective than CRRT in the management of ARF and should be reserved for situations where other modalities of therapy are not available.

of ARF, with decreasing utilization over the past 5–10 years . Drawbacks to the use of PD in ARF are:

(i )low efficiency in fluid and solute removal compared to continous renal replacement therapy CRRT or intermittent hemodialysis (HD)

(ii ) - ARF complicating intra abdominal pathology is unsuitable forPD;

(iii ) - increasing intra abdominal pressure can compromise lung; function use of dialysis fluids with a high dextrose content

may produce hyperglycaemia and other metabolicderangements .

Hemodialysis Ultrafilteration

The main options are peritoneal dialysis, intermittent haemodialysis (HD) combined with ultrafiltration, if necessary intermittent haemofiltration, continuous arteriovenous or venovenous haemofiltration, and haemodiafiltration.

For reasons that are incompletely understood, adverse cardiovascular effects are much less during haemofiltration than during haemodialysis. Continuous treatments are superior to intermittent ones in this respect.

CaseA 19-year-old woman is hospitalized for acute kidney injury (AKI) associated with bloody diarrhea that developed after she returned from a trip to South America. She also has nausea, vomiting, abdominal pain, fever, chills, and decreased urine output. Medical history is otherwise unremarkable, and she takes no medications.On physical examination, temperature is 37.8°C (100.0°F), blood pressure is 135/90 mm Hg, and pulse rate is 110/min. The oral mucosa is dry. There is diffuse abdominal pain with guarding. The remainder of the physical examination is normal.Laboratory studies show haptoglobin 8 mg/dL (80 mg/L), hemoglobin 5.2 g/dL (52 g/L), leukocyte count 20,000/µL (20 × 109/L), platelet count 36,000/µL (36 × 109/L), reticulocyte count 7.8%, serum creatinine 5.7 mg/dL (504 µmol/L) and lactate dehydrogenase 2396 units/L. Peripheral blood smear showed many schistocytes and urinalysis many erythrocytes and erythrocyte casts. Urine protein creatinine ratio is 0.5 mg/mg.

Q: Which of the following is the most likely cause of this patient's acute kidney injury?A. Acute tubular necrosis B. Hemolytic uremic syndrome C. Postinfectious glomerulonephritis D. Scleroderma renal crisis

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