chronic kidney disease darrell gray, ii md internal medicine tenwek hospital
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Chronic Kidney DiseaseChronic Kidney DiseaseChronic Kidney DiseaseChronic Kidney Disease
Darrell Gray, II MDDarrell Gray, II MD
Internal MedicineInternal Medicine
Tenwek HospitalTenwek Hospital
DefinitionsDefinitions
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 does CKD develop?How does CKD develop?How does CKD develop?How does CKD develop?
Common pathway
Initial Pathologic Insult
Reduced Nephron Mass
Glomerular Injury
Growth Promoters Acting on Intact
Glomeruli
End-Stage Kidney
Glomerular Hypertrophy on intact Glomeruli
Ok, but what are the clinical features?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 featuresMore 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 signsMore about metabolic signsMore about metabolic signsMore 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 hyperPTH
Phos
Binders
↓ ↑ ↑↑↑ Severe 2º hyperPTH
Phos binders and Vit D
↑ variable ↓ Excessive Ca/VitD replcmnt
Stop replcmnt
So my pt presents with concerning Hx So my pt presents with concerning Hx and PE. What studies to do I need??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 !!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 FailureCauses of Chronic Renal FailureCauses of Chronic Renal FailureCauses of Chronic Renal Failure
• Glomerulonephritis
• HTN
• Diabetic nephropathy
• Pulmonary-renal syndromes
• Systemic diseases
• Urinary tract pathology
• Congenital
GlomerulonephritidesGlomerulonephritidesGlomerulonephritidesGlomerulonephritides
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 Hypertension / Renovascular DiseaseDisease
Hypertension / Renovascular Hypertension / Renovascular DiseaseDisease
Nephrosclerosis Ischemic Renal Disease
– Abdominal bruits.– Atherosclerotic disease elsewhere.– ARF on ACE inhibitors.
Pulmonary -Renal SyndromesPulmonary -Renal SyndromesPulmonary -Renal SyndromesPulmonary -Renal Syndromes
Goodpasture’s Syndrome (anti-basement membrane disease)
Wegener’s Granulomatosis and other ANCA (antineutrophil cytoplasmic antibody) associated diseases.
Secondary to Systemic DiseasesSecondary to Systemic DiseasesSecondary to Systemic DiseasesSecondary to Systemic Diseases
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 DiseaseUrinary Tract DiseaseUrinary Tract DiseaseUrinary Tract Disease
Reflux Nephritis. Ureteral or Urethral Obstruction. Other causes of chronic or recurrent
obstruction.
CongenitalCongenitalCongenitalCongenital
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 Therapy of Chronic Renal FailureFailure
Therapy of Chronic Renal Therapy of Chronic Renal FailureFailure
Diet TherapyDiet TherapyDiet TherapyDiet 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.
Phosphate ControlPhosphate ControlPhosphate ControlPhosphate Control
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 ControlPTH 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.
HypertensionHypertensionHypertensionHypertension
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?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 recommendationsSummary of recommendations
Aggressive BP control (<130/80)– ACEI or ARB preferred
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)