Objectives

Anatomy Function Chronic Renal Failure (CRF)

Causes Symptoms

Dialysis

Anatomy and Physiology

The Kidneys Hilum Medulla Pyramids Papilla Renal Pelvis

Anatomy

2 Kidneys 2 Ureters Bladder Urethra

Kidney Function

Detoxify blood Increase calcium absorption

calcitriol Stimulate RBC production

erythropoietin Regulate blood pressure and

electrolyte balance renin

Formation of Urine Glomerular Filtration

GFR Reabsorption and Secretion

Simple diffusion and osmosis Facilitated diffusion

Active transport

Azotemia: elevated blood urea nitrogen not from an intrinsic renal disease

Oliguria: urine output less than 500cc/24hr.

Nonoliguria: urine output greater than 500cc/24hr.

Anuria:urine output less than 50cc/24hr.

Acute Versus Chronic Acute

sudden onset rapid reduction in urine output Usually reversible Tubular cell death and regeneration

Chronic Progressive Not reversible Nephron loss

75% of function can be lost before its noticeable

ARF versus CRF

NeuropathyRenal osteodystrophySmall size KidneyPast history of CKDBroad cast

Chronic renal failure

Chronic renal failure: slowly progressive and non- reversible loss of kidney function

Uraemia: metabolic outcome of chronic renal failure

End-stage renal disease: requirement for renal replacement therapy

ETIOLOGY

Diabetes mellitus (28%) Hypertension (25%) Glomerulonephritis (21%) Polycystic Kidney Diease (4%) Other (23%): Obstruction, infection,

etc.

Progression of chronic renal failure

Factors causing progression sustaining primary disease systemic hypertension Intraglomerular hypertension Proteinuria Nephrocalcinosis Dyslipidaemia Imbalance between renal energy demands

and supply

Slowing the Progression of Chronic Renal Failure

Control BP to <130 /80 Diet Anaemia Calcium and Phosphate Dyslipidaemia Obesity Smoking Cessation

Old Chinese saying.……

Good doctor relieve disease

Better doctor cure disease

Superior doctor prevent disease

Symptoms of chronic renal failure

Many are symptom free until 2/3 of renal mass lost. Often no physical examination findings or history. Several common modes of presentation:

progressive lethargy, anorexia, (and later vomiting)

hypertension, and /or heart failure unexplained anaemia serendipitous findings on

biochemistry

The Medical Burden Of Chronic Renal Failure

Prevention of ESRD may prevent other co-morbid conditions from developing

In particular, there is a high prevalence of Cardiovascular diseases in patients with Chronic kidney disease

CHRONIC RENAL FAILURE:CLINICAL MANIFESTATIONS

Sodium and water retention Hyperkalemia Metabolic Acidosis Mineral and Bone metabolism Cardiovascular and Pulmonary Disorders Hematologic Abnormalities Neuromuscular Abnormalities Gastrointestinal Abnormalities Endocrine Abnormalities Dermatologic Abnormalities

Sodium and Volume Balance

Sodium and water retention: CHF, Hypertension, ascites, edema

Enhanced sensitivity to extra-renal sodium and water loss vomiting, diarrhea, fever, sweating Symptoms: dry mouth, dizziness, tachycardia,

etc. Recommendations

Avoid excess salt and water intake Diuretics or dialysis

Potassium Balance

Hyperkalemia (GFR below 5 mL/min) GFRs >5 mL/min: compensatory

aldosterone-mediated K transport in the DCT

K-sparing diuretics, ACEis, beta-blockers impair Aldosterone-mediated actions

Exacerbation of hyperkalenia: Exogenous factors: K-rich diet, etc. Endogenous factors: infection, trauma, etc.

Hyperkalemia & EKG K > 5.5 -6 Tall, peaked T’s Wide QRS Prolong PR Diminished P Prolonged QT QRS-T merge – sine

wave

Hyperkalemia Symptoms Weakness Lethargy Muscle cramps Paresthesias Hypoactive DTRs Dysrhythmias

Metabolic Acidosis

Decreased acid excretion and ability to maintain physiologic buffering capacity:

GFR < 20 mL/min: transient moderate acidosis

Treat with oral sodium bicarbonate Increased susceptibility to acidosis

Mineral and Bone

Bone disease (Figure 16-6) from: Decreased Ca absorption from the gut Over-production of PTH Altered Vitamin D metabolism Chronic metabolic acidosis

Cardiovascular and Pulmonary Abnormalities

Volume and salt overload CHF and pulmonary edema Hypertension

Hyperreninemia: Hypertension Pericarditis: Remic toxin accumulation Accelerated atherosclerosis: linked to

factors above and metabolic abnormalities (Ca alterations, hyperlipidemia)

Hematological Abnormalities

Anemia: lack of erythropoietin production Bone marrow suppression:

uremic poisons: leukocyte suppression - infection

bone marrow fibrosis: elevated PTH an aluminum toxicity from dialysis

Increased bruising, blood loss (surgery) and hemorrhage

Lab Abnormalities: Prolonged bleeding time, abnormal platelet aggregation

Neuromuscular Abnormalites

CNS Abnormalities: Mild-Moderate: Sleep disorders, impaired

concentration and memory, irritability Severe: Asterixis, myoclonus, stupor,

seizures and coma Peripheral neuropathies:

“restless legs” syndrome Hemodialysis-related neuropathies

Gastrointestinal Abnormalities

Peptic Ulcer disease: Secondary hyperparathyrodism?

Uremic gastroenteritis: mucosal alterations

Uremic Fetor: bad breath (ammonia) Non-Specific abnormalities:

anorexia, nausea, vomiting, diverticulosis, hiccoughs

Endocrine Abnormalities

Insulin: Prolonged half-life due to reduced clearance (metabolism)

Amenorrhea and pregnancy failure: low estrogen levels

Impotence, oligospermia and geminal cell dysplasia: Low testosterone levels

Dermatologic Abnormalities

Pallor: anemia Skin color changes: accumulation

of pigments Ecchymoses and hematomas:

clotting abnormalities Pruritus and Excoriations: Ca

deposits from secondary hyperparathyroidism

Conclusion – chronic renal failure

Progressive chronic disease leading to end-state renal failure

Different primary disease can cause chronic renal failure

Diabetic nephropathy is a frequent cause for chronic renal failure

Symptoms can be very different and depend on primary disease and stage of chronic renal failure

Stages of renal failure can be associated with a progressive decrease of GFR

The consequences are complex according to the different function of the kidney and involve many organ systems

Pre-Dialysis Treatment 1. Maintain normal electrolytes a. Potassium, calcium, phosphate are major

electrolytes affected in CRF b. ACE inhibitors may be acceptable in many

patients with creatinine >3.0mg/dL c. ACE inhibitors may slow the progression of

diabetic and non-diabetic renal disease [13] d. Reduce or discontinue other renal toxins

(including NSAIDS) e. Diuretics (eg. furosemide) may help

maintain potassium in normal range f. Renal diet including high calcium and low

phosphate

1. Reduce protein intake to <0.6gm/kg body weight

a. Appears to slow progression of diabetic and non-diabetic kideny disease

b. In type 1 diabetes mellitus, protein restriction reduced levels of albuminuria

c. Low protein diet did not slow progression in children with CRF

1. Underlying Disease

a. Diabetic nephropathy should be treated with ACE inhibitors until creatinine >2.5-3mg/dL

b. Hypertension should be aggressively treated (ACE inhibitors are preferred)

Dialysis

½ of patients with CRF eventually require dialysis

Diffuse harmful waste out of body Control BP Keep safe level of chemicals in body 2 types

Hemodialysis Peritoneal dialysis

Hemodialysis1. Indications a. Uremia - azotemia with symptoms and/or signs b. Severe Hyperkalemia c. Volume Overload - usually with congestive heart

failure (pulmonary edema) d. Toxin Removal - ethylene glycol poisoning,

theophylline overdose, etc. e. An arterio-venous fistula in the arm is created

surgically f. Catheters are inserted into the fistula for blood flow

to dialysis machine

Hemodialysis

3-4 times a week Takes 2-4 hours Machine filters

blood and returns it to body

1. Procedure for Chronic Hemodialysis a. Blood is run through a semi-permeable

filter membrane bathed in dialysate b. Composition of the dialysate is altered to

adjust electrolyte parameters c. Electrolytes and some toxins pass through

filter d. By controlling flow rates (pressures),

patient's intravascular volume can be reduced

e. Most chronic hemodialysis patients receive 3 hours dialysis 3 days per week

1. Efficacy a. Some acids, BUN and creatinine are

reduced b. Phosphate is dialyzed, but quickly

released from bone c. Very effective at reducing

intravascular volume/potassium d. Once dialysis is initiated, kidney

function is often reducede. Not all uremic toxins are removed

and patients generally do not feel "normal"

f. Response of anemia to erythropoietin is often suboptimal with hemodialysis

1. Chronic Hemodialysis Medications a. Anti-hypertensives - labetolol, CCB, ACE

inhibitors b. Eythropoietin (Epogen®) for anemia in

~80% dialysis ptsc. Vitamin D Analogs - calcitriol given

intravenously d. Calcium carbonate or acetate to

phosphate and PTHe. RenaGel, a non-adsorbed phosphate

binder, is being developed for hyperphosphatemia

f. DDAVP may be effective for patients with symptomatic platelet problems

Types of Access Temporary site AV fistula

Surgeon constructs by combining an artery and a vein

3 to 6 months to mature AV graft

Man-made tube inserted by a surgeon to connect artery and vein

2 to 6 weeks to mature

Temporary Catheter

AV Fistula & Graft

Chronic Renal Failure

Long-Term Management Renal Dialysis

Hemodialysis Common

complications

What This Means For You

No BP on same arm as fistula Protect arm from injury Control obvious hemorrhage

Bleeding will be arterial Maintain direct pressure

No IV on same arm as fistula A thrill will be felt – this is normal

Access Problems

AV graft thrombosis AV fistula or graft bleeding AV graft infection Steal Phenomenon

Early post-op Ischemic distally Apply small amount of pressure to

reverse symptoms

Peritoneal Dialysis

Abdominal lining filters blood 3 types

Continuous ambulatory Continuous cyclical Intermittent

Considerations

Make sure the dressing remains intact Do not push or pull on the catheter Do not disconnect any of the

catheters Always transport the patient and

bags/catheters as one piece Never inject anything into catheter

Dialysis Related Problems

Lightheaded –give fluids Hypotension Dysrhythmias Disequilibration Syndrome

At end of early sessions Confusion, tremor, seizure Due to decrease concentration of blood

versus brain leading to cerebral edema