Chronic Renal Failure @

موضوع: Chronic Renal Failure @ الخميس سبتمبر 17, 2009 3:45 pm

Either kidney damage or a decreased kidney glomerular filtration rate (GFR) of <60 mL/min/1.73 m2 for 3 or more months

Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)
Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)
Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2)
Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)
Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis)

Pathophysiology

Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR.
Regardless of the etiology of renal injury, with progressive destruction of nephrons, the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons.

progressive renal injury occurs due to:

Systemic hypertension
Acute insults from nephrotoxins or decreased perfusion
Proteinuria
Increased renal ammoniagenesis with interstitial injury
Hyperlipidemia
Hyperphosphatemia with calcium phosphate deposition
Decreased levels of nitrous oxide

CKD is found in persons of all ages. Nonetheless, in the United States, the highest incidence rate of ESRD occurs in patients older than 65 years.
Besides diabetes mellitus and hypertension, age is an independent major predictor of CKD.

Note that after age 30 years progressive physiological glomerulosclerosis occurs, with GFR (and creatinine clearance [CrCl) falling linearly at a rate of approximately 8 cc/min/1.73 m2/y from a maximal GFR of 140 cc/min/1.73 m2.

Aging also results in concomitant progressive physiological decrease in muscle mass such that daily urinary creatinine excretion also decreases; this combination of factors results in constant serum creatinine values over time in a given individual, despite a decrease in CrCl (and GFR).

Risk Factors

Age > 60 years
Race or ethnic background
African-American
Hispanic
American Indian
Asian
History of exposure to chemicals/toxins
Cigarette smoke
Heavy metals
Family history of chronic kidney disease

Causes of CRF

Diabetic Nephropathy
Hypertension
Vascular Disease
Polycystic Kidney Disease/Genetics
Chronic Inflammation
Obstruction
Glomerular Disorders/ Glomerulonephritis

Chronic vs. Acute Renal Failure

Acute Renal Failure (ARF):
Abrupt onset
Potentially reversible
Chronic Renal Failure (CRF):
Progresses over at least 3 months
Permanent- non-reversible damage to nephrons

Pathophysiology of CRF
Progressive destruction of nephrons leads to:
Decreased glomerular filtration, tubular reabsorption & renal hormone regulation
Remaining functional nephrons compensate
Functional and structural changes occur
Inflammatory response triggered
Healthy glomeruli so overburdened they become stiff, sclerotic and necrotic

Functional Changes of CRF
The Kidneys are unable to:
Regulate fluids and electrolytes
Balance fluid volume and renin-angiotensin system
Control blood pressure
Eliminate nitrogen and other wastes
Synthesize erythropoietin
Regulate serum phosphate and calcium levels

Structural Changes of CRF

Epithelial damage
Glomerular and parietal basement membrane damage
Vessel wall thickening
Vessel lumen narrowing leading to stenosis of arteries and capillaries
Sclerosis of membranes, glomeruli and tubules
Reduced glomerular filtration rate
Nephron destruction

Patients with CKD stage 3 or lower (GFR >30 mL/min) generally are asymptomatic and do not experience clinically evident disturbances in water or electrolyte balance or endocrine/metabolic derangements.
Generally, these disturbances clinically manifest with CKD stages 4 and 5 (GFR <30 mL/min). Uremic manifestations in patients with CKD stage 5 are believed to be primarily secondary to an accumulation of toxins, the identity of which is generally not known.

Hyperkalemia usually develops when GFR falls to less than 20-25 mL/min because of the decreased ability of the kidneys to excrete potassium.
Hyperkalemia in CKD can be aggravated by an extracellular shift of potassium, such as that occurs in the setting of acidemia or from lack of insulin.
Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin,

Platelet disturbance exists with uraemia too
Secondary hyperparathyroidism develops because of hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D, or calcitriol), and hyperphosphatemia.

Other manifestations of uremia in ESRD, many of which are more likely in patients who are inadequately dialyzed, include the following:
Pericarditis - Can complicate with cardiac tamponade, possibly resulting in death
Encephalopathy - Can progress to coma and death
Peripheral neuropathy
Restless leg syndrome
GI symptoms - Anorexia, nausea, vomiting, diarrhea
Skin manifestations - Dry skin, pruritus, ecchymosis
Fatigue, increased somnolence, failure to thrive
Malnutrition
Erectile dysfunction, decreased libido, amenorrhea
Platelet dysfunction with tendency to bleeding

SIGNS & SYMPTOMS

Anemia’s - d/t decreased erythropoietin secretion & uremic toxin damage to RBC’s
Azotemia – (elevated nitrogen) d/t retention of nitrogenous wastes
Creatinine – a component of muscle & it’s non-protein waste product. Normally filtered in the glomerulus & lost in the urine. Glomerular damage increases reabsorption into the blood. Serum creatinine 3 x normal shows a 75% loss of renal function.

Hypocalcemia – impaired regulation of Vitamin D leads to decreased absorption & low calcium levels. High phosphorus levels also cause low serum calcium levels.
Hyperkalemia – impaired excretion of potassium by the kidneys leads to elevated potassium levels.

Hyperlipidemia – decreased serum albumin leads to increased synthesis of LDL’s & cholesterol by the liver, contributing to elevated lipid levels
Proteinuria – increased protein filtration d/t glomeruli damage

Dry mouth, fatigue, nausea – d/t hyponatremia & uremia
Hypertension – d/t sodium & water retention
Hypervolemia – d/t sodium & water retention
Gray/yellow skin – d/t accumulated urine pigments

Cardiac irritability – d/t hyperkalemia
Muscle cramps – d/t hypocalcemia
Bone & muscle pain – d/t hypocalcemia / hyperphosphatemia
Restless leg syndrome – d/t toxins’ effects on the nervous system

Polycystic Kidney Disease

Most Common Genetic Disorder
Numerous fluid-filled cysts in kidneys and renal tubules
Normal renal tissue replaced by cysts
Decreased function leads to end-stage renal disease

Two Major Forms PKD

Autosomal Dominant PKD

Autosomal Recessive PKD

Only treatment for both = dialysis and kidney transplantation

Autosomal Dominant PKD
90% of the cases of PKD are this form
4th leading cause of renal failure age 40-60
Undetected for years until symptoms develop
Occurs equally males and females, mainly Caucasians
One parent with ADPKD gene = 50% chance children will inherit disease
Gene mutation on chromosome 16 or 4
Rare form – occurs in 1 in 4 babies (of parents with mutation)
Worst cases die within hours of birth
Both parents with gene mutation
Mutation on chromosome 6
25% chance children will inherit disease

Imaging Studies:
Plain abdominal x-ray - Particularly useful to look for radio-opaque stones or nephrocalcinosis
Intravenous pyelogram - Not commonly used because of potential for intravenous contrast renal toxicity; often used to diagnose renal stones
Renal ultrasound - Small echogenic kidneys are observed in advanced renal failure. Kidneys usually are normal in size in advanced diabetic nephropathy, where affected kidneys initially are enlarged from hyperfiltration. Structural abnormalities, such as polycystic kidneys, also may be observed. This is a useful test to screen for hydronephrosis, which may not be observed in early obstruction, or involvement of the retroperitoneum with fibrosis, tumor, or diffuse adenopathy. Retrograde pyelogram may be indicated if a high index of clinical suspicion for obstruction exists despite a negative study finding.
Renal radionuclide scan - Useful to screen for renal artery stenosis when performed with captopril administration but is unreliable for GFR of less than 30 cc/min; also quantitates differential renal contribution to total GFR

CT scan - CT scan is useful to better define renal masses and cysts usually noted on ultrasound. Also, it is the most sensitive test for identifying renal stones. IV contrast-enhanced CT scans should be avoided in patients with renal impairment to avoid acute renal failure; this risk significantly increases in patients with moderate-to-severe CKD. Dehydration also markedly increases this risk.

MRI is very useful in patients who require a CT scan but who cannot receive intravenous contrast. It is reliable in the diagnosis of renal vein thrombosis, as are CT scan and renal venography. Magnetic resonance angiography also is becoming more useful for diagnosis of renal artery stenosis, although renal arteriography remains the criterion standard.

Voiding cystourethrogram (VCUG) - Criterion standard for diagnosis of vesicoureteral reflux

Other Tests:
The Cockcroft-Gault formula for estimating CrCl should be used routinely as a simple means to provide a reliable approximation of residual renal function in all patients with CKD. The formulas are as follows:
CrCl (male) = ([140-age] X weight in kg)/(serum creatinine X 72)
CrCl (female) = CrCl (male) X 0.85

Medical Care
Medical care of the patients with CKD should focus on the following:
Delaying or halting progression of CKD
Treatment of the underlying condition if possible
Aggressive blood pressure control to target values per current guidelines

Use of ACE inhibitors as tolerated, with close monitoring for renal deterioration and for hyperkalemia (avoid in advanced renal failure, bilateral renal artery stenosis [RAS], RAS in a solitary kidney)

Aggressive glycemic control per the American Diabetes Association (ADA) recommendations; target HbA1C <7.0%

Protein restriction - Controversial
Treatment of hyperlipidemia to target levels per current guidelines
Avoidance of nephrotoxins - IV radiocontrast, nonsteroidal anti-inflammatory agents, aminoglycosides
Treating pathologic manifestations of CKD, including the following:
Anemia with erythropoietin
Hyperphosphatemia with dietary phosphate binders and dietary phosphate restriction
Hypocalcemia with calcium supplements +/- calcitriol
Hyperparathyroidism with calcitriol or vitamin D analogs
Volume overload with loop diuretics or ultrafiltration
Metabolic acidosis with oral alkali supplementation
Uremic manifestations with chronic renal replacement therapy (hemodialysis, peritoneal dialysis, or renal transplantation): Indications include severe metabolic acidosis, hyperkalemia, pericarditis, encephalopathy, intractable volume overload, failure to thrive and malnutrition, peripheral neuropathy, intractable gastrointestinal symptoms, and GFR less than 10 mL/min.
Cardiovascular complications
Timely planning for chronic renal replacement therapy
Early education regarding natural disease progression, different dialytic modalities, renal transplantation, patient option to refuse or discontinue chronic dialysis
Timely placement of permanent vascular access (arrange for surgical creation of primary arteriovenous fistula, if possible, and preferably at least 6 months in advance of anticipated date of dialysis)
Timely elective peritoneal dialysis catheter insertion
Timely referral for renal transplantation

Consultations:
Early nephrology referral (decreases morbidity and mortality)
Renal dietitian
Vascular surgery for permanent vascular access
General surgery for peritoneal catheter placement
Referral to renal transplant center

Diet:
Protein restriction early in CKD as a means to delay a decline in GFR is controversial; however, as the patient approaches CKD stage 5, this is recommended to delay the onset of uremic symptoms.

Patients with CKD who already are predisposed to becoming malnourished are at higher risk for malnutrition with overly aggressive protein restriction. Malnutrition is a well-established predictor of increased morbidity and mortality in the ESRD population and must be avoided if possible.

Phosphate restriction starting early in CKD
Potassium restriction
Sodium and water restriction as needed to avoid volume overload

>>>>

good luck 4 all

>>

best wishes

AHMED LABEDI

God Protect everyone from this disease
We can protect the kidneys by drinking water
Thanks for the topic

موضوع: رد: Chronic Renal Failure @ الجمعة مارس 19, 2010 6:50 pm

Thanks alot for the topic

May Allah bless you