Download Chronic Kidney Disease

Chronic Kidney Disease
Darrell Gray, II MD
Internal Medicine
Tenwek Hospital
Definitions
CKD = > 3 months of ↓ glomerular filtration rate
(GFR) +/- kidney damage as evidenced by
serology, imaging or pathology
GFR= (140 – age) x LBW (kg) x Constant
serum Creat (in µmol/L)
Constant: 1.23 for men; 1.04 for women
How do we apply GFR? . . . in Staging
How does CKD develop?
Initial Pathologic Insult
Reduced Nephron Mass
Common pathway
Glomerular Injury
Growth Promoters
Acting on Intact
Glomeruli
Glomerular Hypertrophy
on intact Glomeruli
End-Stage Kidney
Ok, but what are the clinical features?
• General
– Malaise, nausea, anorexia, pruritis, metallic taste, uremic
fetor (fishy breath), coma
• By system
– Skin: White crystals in and on skin (uremic frost), dry scaly
skin, easy bruising
– Neurologic: encephalopathy, neuropathy, seizures
– Cardiovascular: HTN, HL, CHF, pericarditis, friction rub
– GI: gastritis, ulcers, AVMs, pancreatitis
More clinical features
– Metabolic: Acidosis, ↑K+, ↑PO4, ↓Ca, ↑PTH
• Acidosis and hyperkalemia can become profound when
GFR< 20
– Hematologic: Anemia, bleeding
• Typically when GFR <30
– Musculoskeletal: Osteomalacia, adynamic bone
disease, metastatic calcifications, mixed bone
disease
– Endocrine: Insulin resistance, growth retardation,
hypogonadism, impotence, infertility
More about metabolic signs

Hyperphosphatemia, Hypocalcemia and
Hypermagnesemia.
– Decreased production of 1,25-dihydroxy vitamin
D3 results in decrease GI Ca++ absorption.
– Decreased ability of the kidney to excrete PO4-.
– These result in a decrease in serum Ca++ which
leads to an increase in PTH which results in
increased bone reabsorbtion of Ca++ in an
attempt to normalize free Ca++ levels and leads to
renal bone disease.

Hyperkalemia
– Gradual decrease in tubular handling of K+ can
result in hyperkalemia.
– Usually occurs when GFR severely reduced (<10
ml/min).
– K+ restriction often needed.
– Diabetics with Type IV RTA / Hyporeninemic
Hypoaldosteroneism can develop hyperkalemia
without a severely depressed GFR.
Calcium
Phos
PTH
Process
Treatment
↓
↓
↑
Vit D def
1,25 OH
Vit D
↓
↑
↑
2º
Phos
hyperPTH Binders
↓
↑
↑↑↑
Severe 2º Phos
hyperPTH binders
and Vit D
↑
variable
↓
Excessive Stop
Ca/VitD
replcmnt
replcmnt
So my pt presents with concerning Hx
and PE. What studies to do I need??
• Labs
– K+, Creatinine, Ca++, Mg, Phos
– Urinalysis
– Strict I/O
– Daily weight
• Imaging
– Kidney ultrasound
• Small kidneys bilaterally
But don’t forget !!
• Medications
– Renally dose medications such as
antibiotics/antiretrovirals, ranitidine, atenolol
– Be extremely cautious with starting an ACEI or ARB.
Talk with consultant.
– Avoid using Morphine as toxic metabolites build up.
– If diuresis is necessary, use lasix if patient has
hyponatremia, and thiazide if pt has hypernatremia
• However, thiazides are not effective when GFR <30
Causes of Chronic Renal Failure
•
•
•
•
•
•
•
Glomerulonephritis
HTN
Diabetic nephropathy
Pulmonary-renal syndromes
Systemic diseases
Urinary tract pathology
Congenital
Glomerulonephritides


Idiopathic Membranous
Glomerulonephritis.
Focal and Segmental Glomerulonephritis
(FSGS)



Associated with HIV
IgA Nephropathy (Berger’s Disease).
Membranoproliferative
Glomerulonephritis Type I and II (MPGN I
and II).
Hypertension / Renovascular
Disease


Nephrosclerosis
Ischemic Renal Disease
–
–
–
Abdominal bruits.
Atherosclerotic disease elsewhere.
ARF on ACE inhibitors.
Pulmonary -Renal Syndromes


Goodpasture’s Syndrome (anti-basement
membrane disease)
Wegener’s Granulomatosis and other
ANCA (antineutrophil cytoplasmic
antibody) associated diseases.
Secondary to Systemic Diseases

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Systemic Lupus Erythematosis (SLE).
Other collagen vascular diseases.
Microscopic polyarteritis (vasculitis).
Thrombotic Microangiopathies (HUS, TTP,
PSS, malignant HTN).
Multiple Myeloma (MM).
Amyloidosis
Henoch-Schonlien Purpura (HSP).
Aids Nephropathy.
Urinary Tract Disease



Reflux Nephritis.
Ureteral or Urethral Obstruction.
Other causes of chronic or recurrent
obstruction.
Congenital

Adult Polycystic Kidney Disease (APKD).
– Most common inherited form of renal disease.
– Characterized by numerous cysts in both
kidneys.
– Cysts can also be present in liver, pancreas,
ovaries.
– Other findings can include mitral valve prolapse,
cerebral aneurysms, diverticular disease.

Alport’s Syndrome.
Therapy of Chronic Renal
Failure
Diet Therapy



Low sodium diet for blood pressure and
volume control.
Maintain adequate nutrition.
No proof that low protein (< 0.8 g ptn / kg /
day) slows progression although it may
help in management of acidosis.



May need to use diuretics and fluid
restrict for volume control.
Potassium restriction as needed.
Cholesterol treatment may be required.
One Suggested Approach
Phosphate Control

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Dietary phosphate should be restricted.
Phosphate binders must be given with meals.
Calcium carbonate usually first choice, but as disease
progresses may need to switch to calcium acetate or
non calcium containing binders such as sevelamer or
lanthanum carbonate.
Aluminum hydroxide binders should be avoided if
possible.
– Use with citrate solutions has resulted in aluminum
toxicity and death.
PTH Control
• Use of vitamin D analogs often needed to
reduce iPTH levels (calcitriol, paracalcitol or
doxercalciferol).
• In addition, calcimimetic such as cinacalcet may
also be needed to lower iPTH.
• Issues currently revolve around iPTH/Ca/PO4
and cardiac risk.
Hypertension

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Good control of blood pressure can slow
progression of renal failure.
Evidence that early use of ace inhibitors in Type I
diabetics with nephropathy slows the progression
of renal disease.
Evidence to suggest this also applies to Type II
diabetics.
Evidence for ARBs as first line in Type II diabetics.
Often used interchangeably or in combination.
What Does Good Care do?
Diabetic renal disease progression can be
decreased from 12 ml/min/year to 4 ml/min/year.
Non diabetic renal disease progression can be
slowed from 4-6 ml/min/year down to 2
ml/min/year.
These results are in established chronic disease
with no active primary process.
Summary of recommendations
 Aggressive BP control (<130/80)
– ACEI or ARB preferred
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Excellent control of DM (HgBA1C<7%)
Avoid renal insults (nephrotoxins, etc)
Cardiovascular disease prevention (lipids, etc)
Monitor for anemia
Minimize bone disease
Appropriate nutritional counseling
Smoking cessation (for everybody, not just renal patients)
Early referral to nephrologist (Cr>1.7)