1. Renal failure

2. 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.

3. 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.

4. • 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

5. ACUTE RENAL FAILURE

6. 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).

7. • 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.

8. Causes of ARF
- Pre-renal cause.
- Intrinsic renal cause.
- Post-renal cause.
- Systemic diseases
acting via one or more of these 3 categories.

9. Causes of ARF
Acute Renal Failure
Pre-renal Intrinsic renal Post-renal
Tubular Interstitial Glomerular Vascular

10. nephron
the functional unit of the kidney
•capable of forming urine
•has two major components:
glomerulus
tubule:
proximal
loop of Henle
distal
collecting

11. Causes of ARF
Pre-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

12. Causes of ARF
Pre-renal ARF
I. 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.

13. Causes of ARF
Pre-renal ARF
III.Arterial occlusion (Renal artery occlusion stenosis):
Bilateral thromboembolism.
Thromboembolism of a solitary kidney.

14. 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%

15. Causes of ARF
Intrinsic Renal Causes
I-. 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)

16. • 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 ).

17. Causes of ARF
Intrinsic Renal Causes
II. 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

18. Causes of ARF
Intrinsic Renal Causes
III. Disease of glomeruli ( Acute Glomerulonephritis)
Postinfectious Glomerulonephritis.
Anti-basement membrane antibody disease

19. Causes of ARF
Intrinsic Renal Causes
IV. Vascular :
Vasculitis.
Malignant hypertension.
Microscopic polyarteritis.

20. 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 .

22. 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.

23. 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 .

24. 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..

25. • 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

26. 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.

27. 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

28. 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.

29. 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