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CHRONIC RENAL FAILURE

Lecturer prof. Yu.R. Kovalev

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Over 50% of cases of chronic renal failure
are due to diabetes mellitus and
hypertension. Glomerulonephritis, cystic
diseases, and other urologic diseases
account for another 20-25%, and nearly
one-sixth of patients have unknown
causes.

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COMMON CAUSES
1. Primary glomerular diseases (glomerulonephritis,
IgA nephropathy a.o.)
2. Secondary glomerular diseases (diabetic
nephropathy, amyloidosis, collagen vascular
diseases a.o.)
3. Tubulointerstitial nephritis (drug hypersensitivity,
heavy metals a.o.)
4. Hereditary diseases (polycystic kidney disease a.o.)
5. Obstructive nephropathies (prostatic disease,
nephrolithiasis, tumor, congenital)
6. Vascular diseases (hypertensive nephrosclerosis,
renal artery stenosis) 3
PATHOGENESIS
Chronic renal disease is rarely reversible and leads
to progressive decline in renal function. This occurs
even after an inciting event has been removed.
Reduction in renal mass leads to hypertrophy of the
remaining nephrons with hyperfiltration, and the
glomerular filtration rate in these nephrons are
transiently at supranormal levels. These adaptations
place a burden on the remaining nephrons and lead
to progressive glomerular sclerosis and interstitial
fibrosis, suggesting that hyperfiltration may worsen
renal function.
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PATHOGENESIS
Chronic renal failure is due to progressive destruction of
nephrons. As the nephrons are destroyed, the
parenchyma shrinks and it is replaced by fibrosis. The
remaining nephrons undergo hypertrophy. This gives the
appearance of a granulur contracted kidney. Renal
function is maintained by the hypertrophied nephrons.
Since the concentrating fund ion is impaired, adjustment
of urine volume becomes defective and polyuria with
urine of specific gravity around 1010 occurs. The blood
pressure goes up progressively and this form of
secondary hypertension exerts its deleterious influence
on the kidney, heart, and brain. 5
GLOMERULAR DYNAMICS
Angiotensin II produced locally modulates intraglomerullar
capillary pressure and GFR. Angiotensin II predominantly causes
vasoconstriction of postglomerular arterioles, thereby increasing
the glomerular hydraulic pressure and filtration fraction.

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Effect of the renin-angiotensin system
CLINICAL FEATURES
Organ System Symptoms – Signs
General Fatigue, weakness – Sallow-appearing, chronically ill

Skin Pruritus, easy bruisability – Pallor, ecchymoses, excoriations,


edema, xerosis
ENT Metallic taste in mouth, epistaxis – Urinous breath
Eye Pale conjunctiva
Pulmonary Shortness of breath,– Rales, pleural effusion
Cardiovascular Dyspnea on exertion, retrosternal pain on inspiration (pericarditis) –
Hypertension, cardiomegaly, friction rub
Gastrointestinal Anorexia, nausea, vomiting, hiccup
Genitourinary Nocturia, – Isosthenuria
Neuromuscular Restless legs, numbness and cramps in legs
Neurologic Generalized irritability and inability to concentrate, – Stupor, tremor,
myoclonus, peripheral neuropathy 7
Intercurrent factors precipitate the
development of advanced renal failure
•electrolyte imbalance,
•infection,
•cardiac failure,
•trauma,
•blood loss,
•excessive protein intake,
•alcoholic bouts,
•use of nephrotoxic drugs

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ADDITIONAL SIGNS
Anemia (normochromic, normocytic), erythropoetin ↓
Sometimes iron deficient (bleeding)
Renal osteodystrophy (calcium ↓, phosphorus ↑)
Metabolic acidosis
Hypertension (may be malignant) – salt and water
retention
Uremic encephalopthy
Uremic coagulopathy (platelet disfunction)
Accelerated rate of atherosclerosis (hyperlipidemia)
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ESTABLISHING THE ETIOLOGY
Of special importance in establishing the etiology of
CRF are a history of hypertension; diabetes;
systemic infectious, inflammatory, or metabolic
diseases; exposure to drugs and toxins; and a family
history of renal and urologic disease. Drugs of
particular importance include analgesics (usage
frequently underestimated or denied by the patient),
NSAIDs, gold, penicillamine, antimicrobials, lithium,
and ACE inhibitors. In evaluating the uremic
syndrome, questions about appetite, diet, nausea,
vomiting, hiccup, shortness of breath, edema,
weight change, muscle cramps, bone pain, mental
acuity, and activities of daily living are helpful. 10
URINE EXAMINATION
Urine volume is high (2—3 litres in 24 h). Mild
proteinuria may be evident. The most
remarkable feature is the fixed specific gravity
around 1010 (isosthenuria) and an osmolality
of 300 mOsm/kg water. The presence of broad
casts in urine confirms the chronic nature of
the illness. The estimation of urinary loss of
sodium helps in identifying saltlosing states.

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BLOOD EXAMINATION
Blood urea, serum creatinine, serum uric acid,
and inorganic phosphates are elevated.
Potassium balance generally remains intact in
chronic renal failure until the GFR is less than
10-20 mL/min. In terminal stage potassium
level is increased.
Calcium and bicarbonate levels are reduced.

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IMAGING
Ultrasonography of the abdomen help in
revealing the small size of the kidneys. The
findings of small echogenic kidneys
bilaterally (< 8,5 cm) by ultrasonography
supports a diagnosis of chronic renal failure,
though normal or even large kidneys can be
seen with chronic renal failure caused by
adult polycystic kidney disease, diabetic
nephropathy, HIV-associated nephropathy,
multiple myeloma, amyloidosis, and
obstructive uropathy. 13
DIAGNOSIS
The diagnosis of renal failure is made by
documenting elevations of the urea and
serum creatinine concentrations. The
urinanalysis shows isosthenuria if tubular
concentrating and diluting ability are
impaired. The urinary sediment can show
broad waxy casts as a result of dilated,
hypertrophic nephrons.

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DIAGNOSIS
Evidence of previously elevated urea and creatinine,
abnormal prior urinalyses, and stable but abnormal
serum creatinine on successive days is most
consistent with a chronic process.
The most classic constellation of laboratory and
imaging findings that distinguishes progressive CRF
from acute renal failure are bilaterally small (<8.5
cm) kidneys, anemia, hyperphosphatemia and
hypocalcemia with elevated PTH levels, and a
urinary sediment that is inactive or reveals
proteinuria and broad casts.
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POSSIBLY REVERSIBLE CAUSES
Reversible Factors Diagnostic Clues
Infection Urine culture and sensitivity tests

Obstruction Bladder catheterization, then


renal ultrasound
Extracellular fluid volume depletion Orthostatic blood pressure and
pulse: BP ↓ and pulse ↑ upon
sitting up from a supine position
Hypokalemia, hypercalcemia, and Serum electrolytes, calcium,
hyperuricemia (usually >15mg/dL) phosphate, uric acid
Nephrotoxic agents Drug history
Pericarditis, congestive heart Echocardiography, physical
failure examination, chest x-ray
Hypertension Blood pressure 16
KIDNEY BIOPSY
It should be reserved for patients with near-
normal kidney size, in whom a clearcut diagnosis
cannot be made by less invasive means, and
when the possibility of a reversible underlying
disease process remains tenable so that
clarification of the underlying etiology may alter
management. The extent of tubulointerstitial
scarring on kidney biopsy generally provides the
most reliable pathologic correlate indicating
prognosis for continued deterioration toward
ESRD. 17
DIETARY MANAGEMENTCONTROL OF
HYPERTENSION
1. Protein restriction —Protein intake should not
exceed 1 g/kg/d, and if protein restriction proves to be
beneficial, it should not exceed 0.6 g/kg/d.
2. Salt and water restriction - For the nondialysis
patient approaching end-stage renal disease, 2 g/d of
sodium. A daily intake of 1-2 L of fluid maintains water
balance.
3. Potassium restriction - Restriction is needed once
the GFR has fallen below 10-20 mL/min less than 60-
70 meq/d.
4. Phosphorus restriction
5. Magnesium restriction 18
INDICATIONS FOR DIALYSIS
Renal replacement therapy should not be initiated when
the patient is totally asymptomatic; however, dialysis
and/or transplantation should be started sufficiently early
to prevent serious complications of the uremic state.
Clear indications for initiation of renal replacement
therapy include pericarditis, progressive neuropathy
attributable to uremia, encephalopathy, muscle
irritability, anorexia and nausea that is not ameliorated
by reasonable protein restriction, and fluid and
electrolyte abnormalities that are refractory to
conservative measures. Serum creatinine must be >700
µ mol/L (>8.0 mg/dL) and the creatinine clearance must 19
be <0.17 mL/s (<10 mL/min).
ARTERIOVENOUS FISTULA

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INTRAVENOUS CANNULA IN THE
WRONG PLACE

This patient is right-handed.


Non work arm must kept for arterio-venous fistula
and it must not made any i/v injection there. 21
PROGNOSIS
Patients undergoing dialysis have an average
life expectancy of 3-4 years. The most
common cause of death is cardiac
dysfunction (48%). Other causes include
infection (15%), cerebrovascular disease (6%),
and malignancy (4%). Diabetes, age, a low
serum albumin, lower socioeconomic status,
and inadequate dialysis are all significant
predictors of mortality.
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KIDNEY TRANSPLANTATION
Up to one-half of all patients with end-stage renal
disease are suitable for transplantation. Age is becoming
less of a barrier. Two-thirds of kidney transplants come
from cadaveric donors; the remainder from living related
or unrelated donors. Immunosuppressive drugs include
corticosteroids, azathioprine, cyclosporine a.o. A patient
with a cadaveric renal transplant typically requires
stronger immunosuppression than patients with living
related kidney transplants. However, this depends to a
great extent on the degree of HLA-type matching. 5-year
survival rates 72% for living related and living unrelated
donor transplants and 58% for cadaveric donor
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transplants.