Renal failure

Function of the kidneys

The kidneys are responsible for:

1- removing wastes from the body.

2-regulating electrolyte balance and blood pressure.

3- converting Vit D into its active form.

4-stimulating RBC production by synthesizing erythropoietin.

Renal failure

• Failure of the excretory function of the kidneys,leading to retention of nitrogenous waste products of metabolism.

• Failure of the regulation of fluid & electrolytes status .

• Failure of the endocrine function of the kidney.

• Acute renal failure : Refers to a sudden and usually reversible loss of renal function,

which develops over a period of days or weeks.

• Chronic renal failure : Refers to an irreversible deterioration in renal function which

classically develops over a period of years

ACUTE RENAL FAILURE

ACUTE RENAL FAILURE

Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function ( rapid decline in glomerular filtration rate), which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume.

(>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.

There are many possible causes and it is frequently multifactorial. The clinical picture is often dominated by the underlying condition (e.g. septic shock, trauma).

• ARF complicates approximately 5% of hospital admissions and up to 30% of admissions to intensive care units.

• Oliguria (urine output 400 mL/d) is a frequent but not invariable clinical feature (50%).

• ARF is usually asymptomatic and diagnosed when biochemical monitoring of hospitalized patients reveals a recent increase in blood urea and creatinine concentrations.

Causes of ARF

- Pre-renal cause.

- Intrinsic renal cause.

- Post-renal cause.

- Systemic diseases acting via one or more of these 3 categories.

Causes of ARF

Acute Renal Failure

Pre-renal Intrinsic renal Post-renal

Tubular Interstitial VascularGlomerular

nephron

the functional unit of the kidney

•capable of forming urine

•has two major components:

glomerulus

tubule:proximalloop of Henledistalcollecting

Causes of ARFPre-renal ARF

• Accounts for 60-70% of cases of ARF

• Represents physiologic response to mild-moderate renal hypoperfusion

• Renal parenchymal tissue is not damaged therefore rapidly reversible upon restoration of RBF and glomerular filtration pressure

• Elderly and those with pre-existing renal disease at increased risk

Causes of ARF

Pre-renal ARFI. Absolute decrease in effective blood volume( Hypovolemia):• A. Hemorrhage, burns, dehydration• B. GI fluid loss: vomiting, surgical drainage, diarrhea• C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus),

hypoadrenalism• D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns,

severe hypoalbuminemia

II.Relative decrease in blood volume ( ineffective arterial volume ) Hypotention. • A.Congestive heart failure • B. Systemic vasodilatation: sepsis, antihypertensives, , anaphylaxis .• C.Liver failure. • E. massive pulmonary embolus.

Causes of ARF

Pre-renal ARFIII.Arterial occlusion (Renal artery occlusion\ stenosis):

Bilateral thromboembolism.

Thromboembolism of a solitary kidney.

Causes of ARF

Intrinsic Renal Causes

• Accounts for 25-40% of cases of ARF• Types:– ATN ( Acute Tubular Necrosis ) 85%– Interstitial nephritis 10%– Acute glomerulonephritis <5%– Intrarenal vascular disease <5%

Causes of ARF

Intrinsic Renal CausesI-. Acute tubular necrosis A. Ischemia B. Nephrotoxins C.Sepsis syndrome

• A. Ischemia As for severe prerenal ARF (hypovolemia, low cardiac output, renal

vasoconstriction, systemic vasodilatation), obstetric complications (abruptio placentae, postpartum hemorrhage)

• B. Nephrotoxins 1. Exogenous: Antibiotics (aminoglycosides, cephalosporin , amphotericin B ) Iodinated contrast agents. Chemotherapy (e.g., cisplatin ) Organic solvents (e.g., ethylene glycol) • 2. Endogenous: Intratubular pigments ( hemoglobinuria as in hemolysis, myoglobinuria as in

rhabdomyolysis).

Intratubular proteins (myeloma) .

Intratubular crystals( uric acid, oxalate) ( tumor lysis syndrome ).

Causes of ARF

Intrinsic Renal CausesII. Interstitial nephritis

• A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifampicin), nonsteroidal anti-inflammatory agents, diuretics, captopril

• B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g., cytomegalovirus), fungal (e.g., candidiasis)

• C. Infiltration: lymphoma, leukemia, sarcoidosis

• D. Idiopathic

Causes of ARF

Intrinsic Renal CausesIII. Disease of glomeruli ( Acute Glomerulonephritis)

Postinfectious Glomerulonephritis.

Anti-basement membrane antibody disease

IV. Vascular :

Vasculitis. Malignant hypertension. Microscopic polyarteritis.

Causes of ARF

Intrinsic Renal Causes

Causes of ARF

Post-renal Causes of ARF • Account for 5% of cases of ARF• ARF occurs when both urinary outflow tracts are obstructed or when one

tract is obstructed in a patient with a single functional kidney.

-Bladder outlet obstruction

-Bilateral ureteral obstruction ( unusual ). Ureteral obstruction in a solitarey kidney. ( obstruction by : Calculi, blood clot, sloughed papillae, cancer, external

compression e.g., retroperitoneal fibrosis)

-Urethra stricture .

Types of Acute Renal Failure

• REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE When haemodynamic disturbances produce acute renal

dysfunction that has the potential to be rapidly reversed ( reversable ),by early recognition and treatment .

• ESTABLISHED ACUTE RENAL FAILURE (ATN ) May develop following severe or prolonged under-perfusion of

the kidney (pre-renal ARF). In such cases, the histological pattern of acute tubular necrosis is

usually seen.

REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE

When haemodynamic disturbances produce acute renal dysfunction that has the potential to be rapidly reversed

( reversable ),by early recognition and treatment .

REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE

• Pathogenesis The kidney can regulate its own blood flow and GFR over a wide range of

perfusion pressures. When the perfusion pressure falls-as in hypovolaemia, shock, heart failure or

narrowing of the renal arteries-the resistance vessels in the kidney dilate to facilitate flow. Vasodilator prostaglandins are important.

( this mechanism is markedly impaired by NSAIDs ).

If autoregulation of blood flow fails, the GFR can still be maintained by selective constriction of the post-glomerular (efferent) arteriole. This is mediated through the release of renin and generation of angiotensin II, which preferentially constricts this vessel. (ACE inhibitors interfere with this response) .

More severe or prolonged under-perfusion of the kidneys may lead to failure of these compensatory mechanisms and hence an acute decline in GFR..

• The renal tubules are intact and become hyperfunctional; that is, tubular reabsorption of sodium and water is increased, partly through physical factors associated with changes in blood and urine flow and partly through the influence of angiotensins, aldosterone and vasopressin.

• This leads to the formation of a low volume of urine which is concentrated (osmolality > 600 mOsm/kg) but low in sodium (< 20 mmol/l).

• These urinary changes may be absent in patients with impaired tubular function, e.g. pre-existing renal impairment, or those who have received loop diuretics

Clinical assessment • Features of the underlying cause• There may be marked hypotension and signs of poor peripheral

perfusion, such as delayed capillary return. • Pre-renal ARF may occur without systemic hypotension, particularly

in patients taking NSAIDs or ACE inhibitors . • Postural hypotension (a fall in blood pressure > 20/10 mmHg from

lying to standing) is a valuable sign of early hypovolaemia.

• The cause of the reduced renal perfusion may be obvious, but concealed blood loss can occur into the gastrointestinal tract, following trauma (particularly where there are fractures of the pelvis or femur) and into the pregnant uterus.

• Large volumes of intravascular fluid are lost into tissues after crush injuries or burns, or in severe inflammatory skin diseases or sepsis.

• Metabolic acidosis and hyperkalaemia are often present.

DIAGNOSIS OF PRE-RENAL ACUTE RENAL FAILURE:

- A compatable history.( bleeding , burn , dehydration……)

- The clinical findings.( hypotention , decrease urine output , metabolic acidosis …)

- A progressive increase in blood urea & plasma creatinine. hyperkalemia.

- Urine osmolality > 600 mOsm/kg Urine sodium < 20 mmol/l. Urine/plasma urea ratio of > 10:1

MANAGEMENT OF PRE-RENAL ACUTE RENAL FAILURE:

• Establish and correct the underlying cause of the ARF.

• If hypovolaemia is present, restore blood volume as rapidly as possible (with blood, plasma or isotonic saline (0.9%), depending on what has been lost).

• Monitoring of the central venous pressure or pulmonary wedge pressure as an adjunct to clinical examination may aid in determining the rate of administration of fluid.

• Critically ill patients may require invasive haemodynamic monitoring to assess cardiac output and systemic vascular resistance, and the use of inotropic drugs to restore an effective blood pressure .

• Correct metabolic acidosis. – Restoration of blood volume will correct acidosis by restoring kidney function. – Isotonic sodium bicarbonate (e.g. 500 ml of 1.26%) may be used.

PROGNOSIS OF PRE-RENAL ACUTE RENAL FAILURE

• If treatment is given sufficiently early, renal function will usually improve rapidly; in such circumstances residual renal impairment is unlikely.

• In some cases, however, treatment is ineffective and renal failure becomes established