Chronic renal failure

Chronic kidney disease (CKD)

Progressive loss of renal function over time; based on a gradual decline in the GFR and creatinine
clearance. The diagnosis of CKD requires the following:

1. Decline of kidney function for 3 months or more AND

2. Evidence of kidney damage (e.g. albuminuria or abnormal biopsy) OR
GFR <60 mL/min/1.73 m2

End stage renal disease- The final “stage” of CKD in which the patient is dependent on dialysis for
survival. The number 1 cause of ERSD is diabetes mellitus combined with hypertension.

Classifying CKD

 Stage 1: Kidney damage with normal or increased GFR (>90-120 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) – prepared for transplant or dialysis
 Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis) – requires transplant or dialysis

Epidemiology

CKD is more common in men, African-native- and Asian-Americans and thos between the ages of 45 and
64 years.

People with high blood pressure and diabetes are also at high risk of suffering from CKD than those
people without these underlying conditions. About one of five adults with hypertension and one of
three adults with diabetes have CKD. Other health conditions that may lead to CKD are obesity, high
cholesterol, a family history of the disease, lupus, and other forms of cardiovascular diseases.

Etiology

Chronic kidney disease occurs when a disease or condition impairs kidney function, causing kidney
damage to worsen over several months or years. Diseases and conditions that cause chronic kidney
disease include:

Signs and Symptoms

Patients appear ill and anemic and also develop nocturia

Hyperpigmentation of skin characterized by a brownish-yellow appearance

Uremic frost

GI signs such as anorexia, nausea and vomiting, generalized gastroenteritis and peptic ulcer disease

Convulsions

Stomatitis

Gastrointestinal bleeding

Epistaxis

Cardiovascular manifestations

Pathophysiology

Patients with stages 1-3 ([GFR] >30 mL/min) of CKD are generally asymptomatic; water/electrolyte
imbalances or endocrine/metabolic derangements are not clinically evident.

These disturbances manifest clinically in CKD stages 4-5 (GFR < 30 mL/min).

Sign/lab finding Symptoms Mechanism

Generalized edema Swelling Water retention due to a loss of GFR
leading to sodium and fluid
retention. Fluid moves into the
extravascular space, due to
increased hydrostatic pressure,
causing pitting edema in the lower
extremity (fluid movement could
also be due to hypoalbuminemia, in
some diseases, leading to a low
oncotic pressure).
Pulmonary crackles Shortness of Fluid accumulation causes
breath pulmonary edema and loss of air
space causing ventilation-perfusion
mismatch. This leaves less area for
oxygen diffusion form the blood
vessels.
Anemia Fatigue, Erythropoietin (EPO), the major
reduced erythropoiesis stimulator, is released
( normocytic exercise from the kidneys; with renal failure,
anemia ) capacity, and there is loss of EPO release.
pallor
Weight loss Loss of lean Protein-energy malnutrition due to
body mass metabolic acidosis. Loss of kidney
function results in impaired H+
secretion from the body.
Hyperkalemia Malaise, Inability of the kidneys to secrete
palpitations potassium in the urine leads to life
threatening arrhythmias

Metabolic Acidosis
Mechanisms of renal osteodystrophy
Hyperphosphatemia Damaged kidneys fail to excrete
phosphate.

Also secondary to high parathyroid

hormone levels.
Hypocalcemia Thought to be secondary to low
Vitamin D3 levels. In early stages of
CKD, low levels of calcitriol are due
to hyperphosphatemia (negative
feedback). In the later stages of CKD,
low levels are hypothesized to be
due to decreased synthesis of 1α-
hydroxylase (enzyme that converts
calcifediol to calcitriol in the
kidneys).
Secondary and To compensate for the low calcium
tertiary due to low Vitamin D levels, the
hyperparathyroidism parathyroid glands increase the
parathyroid hormone secretion. This
leads to a high bone turnover,
always attempting to normalize the
low calcium levels in the blood. Over
time, this becomes maladaptive
leading to extraosseous calcification,
and parathyroid hyperplasia
develops (tertiary
hyperparathyroidism).
Complications of uremia

Urea and other toxins accumulate in the blood and cause life threatening
issues.
Ecchymosis, GI Increased Uremia-induced platelet dysfunction
bleeding tendency to
bleed and
ecchymosis
Pericardial friction Chest pain, Uremic pericarditis
rub malaise
Encephalitis Headaches, Uremic encephalopathy; adverse
confusion, effects of urea on the CNS.
coma

Diagnosis

Laboratory studies used in the diagnosis of CKD can include the following:

 Complete blood count (CBC)

 Basic metabolic panel
 Urinalysis
  Serum albumin levels: Patients may have hypoalbuminemia due to malnutrition, urinary protein
loss, or chronic inflammation
 Lipid profile: Patients with CKD have an increased risk of cardiovascular disease
 Page 151 medcom

Evidence of renal bone disease can be derived from the following tests:

 Serum calcium and phosphate

 25-hydroxyvitamin D
 Alkaline phosphatase
 Intact parathyroid hormone (PTH) levels

Imaging studies

Imaging studies that can be used in the diagnosis of CKD include the following:

 Renal ultrasonography: Most useful imaging study. Determines the presence of two kidneys,
determines if they are symmetric, provides an estimate of kidney size and rule out renal masses
and evidence of obstruction
 Retrograde pyelography: Useful in cases with high suspicion for obstruction despite negative
renal ultrasonograms, as well as for diagnosing renal stones
 Computed tomography (CT) scanning: Useful to better define renal masses and cysts usually
noted on ultrasonograms; also the most sensitive test for identifying renal stones
 Magnetic resonance imaging (MRI): Useful in patients who require a CT scan but who cannot
receive intravenous contrast; reliable in the diagnosis of renal vein thrombosis

Biopsy

Biopsy is not advised in patients with bilaterally small kidneys since 1.) it is technically difficult and has
greater likelihood of causeing bleeding 2.) there is usually so much scarring that the underlying dse may
not be apparent 3.) the window of opportunity to render disease specific therapy has passed.

Percutaneous renal biopsy is generally indicated when renal impairment and/or proteinuria approaching
the nephrotic range are present and the diagnosis is unclear after appropriate workup.

Differential Diagnosis

It is important to differentiate CKD from acute kidney injury (AKI) because AKI can be reversible.
Abdominal ultrasound, in which the size of the kidneys is measured, is commonly performed. Kidneys
with CKD are usually smaller (≤ 9 cm) than normal kidneys, with notable exceptions such as in early
diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD
from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden
increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the
patient has been well and has had no blood tests), it is occasionally necessary to treat a patient briefly as
having AKI until the kidney impairment has been established to be irreversible.Evidence of metabolic
bone disease with hyperphosphotemia, hypocalcemia and elevated PTH suggest chronicity. Normocytic,
normochromic anemia suggest the process has been going for some time.

Management
Delaying or halting the progression of CKD: Treatment of the underlying condition, if possible, is
indicated
Diagnosing and treating the pathologic manifestations of CKD
Timely planning for long-term renal replacement therapy

Control of blood pressure and treatment of the original disease are the broad principles of management.

 Cardiovascular disease (CVD)is the leading cause of death in patients with CKD.
o Reducing risk factors for development of CVD is beneficial.
 E.g. treatment of hyperlipidemia, lifestyle and dietary changes
 Tight blood pressure control:
o Reducing damage due to the end organ effects of hypertension on the kidney as well as
the heart.
o Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor
blockers(ARBs) block the effects of angiotensin II on (i) sodium and fluid retention, (ii)
vasoconstriction, (iii) stimulating ADH release, (iv) stimulating aldosterone release, and
(v) inducing a sympathetic response.
 ACEIs and ARBs also slow down progression of proteinuria in patients with
diabetic CKD.
 Diabetes management:
o Tight glucose management slows the progression of vascular and heart disease.
 Avoidance of IV contrast, NSAIDs, and nephrotoxic drugs:
o These agents can potentially induce an acute kidney injury (AKI) on the underlying
kidney disease and therefore exacerbate the baseline CKD.
 Diet:
o The intake of sodium usually is not restricted unless fluid accumulations and is retained
or high blood pressure develops.
o Occasionally, water intake needs to be restricted to prevent the sodium conc. From
becoming too low
o Foods high in potassium such as salt substitutes must be avoided. Food high in
potassium such as dates and figs should not be consumed in excess. A high potassium in
the blood increases risk of abnormal heart rhythms.

Renal transplant and Dialysis

Dialysis is a medical procedure that artificially filters blood. It becomes necessary when the number of
nephrons diminishes to the point that azotemia is unpreventable or uncontrollable.

There are two kinds of dialysis. In hemodialysis, blood is pumped out of your body to an artificial kidney
machine, and returned to your body by tubes that connect you to the machine. In peritoneal dialysis,
the peritoneum- a membrane that lines the abdomen and covers the abdominal organs - acts as a
natural filter.

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