Table of contents
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Chronic Kidney Disease
See KDIGO guidelines 2012 on management for details
For KDIGO guidelines 2012 click HERE
External Link: KDIGO.ORG CKD Section
Hypertension
- Managing hypertension is indicated for all patients with kidney disease. (regardless of etiology)
- Controlling blood pressure helps to decrease cardiovascular risk and may help to prevent progression to end-stage kidney disease.
- ACEi/ARB are preferred Anti-HTN agents in CKD, especially in those with proteinuria.
- Mechanism:
- ACEi/ARB lower efferent arteriolar resistance and lower intraglomerular pressure.
- The lower intraglomerular pressure is thought to be protective for the kidney but may be associated with a slight increase in the serum creatinine level (30% increase is acceptable).
- CAUTION: Use of these agents also may cause hyperkalemia. Use diuretics to manage hyperkalemia, further HTN, and edema.
- Higher doses of diuretics are often required.
Metabolic Acidosis
- Metabolic acidosis develops when GFR delines (usually < 30)
- de Brito-Ashurst et al (2009): RCT comparing sodium bicarb to no treatment.
- Treatment had lower annual decline in renal function, lower creat, less dialysis.
- Many had concerns over sodium load, but BP did NOT increase in the study.
- Therefore: use sodium bicarb to target HCO3 of >22 mEq/L in patients with metabolic acidosis and GFR < 30 (Stage IV CKD)
- Benefits: slows progression of CKD, slows metabolic bone disease, improves nutrition status.
Chronic Tubulointerstitial Disorders
- Can evolve from Acute Interstitial Nephritis
- Damage to the tubules and interstitium
Investigations
- Low Hb (Epo producing cells destroyed)
- Urine:
- Urinalysis - bland or sterile pyuria
- Urine Protein - usually low-molecular weight (<2g/24hrs)
- Ultrasound - small atrophic kidneys
- Biopsy Indications:
- Unclear Etiology (possible change in therapy based on results)
Causes
Causes of Chronic Tubulointerstitial Disorders
| Category | Explanation | ||
|---|---|---|---|
| Autoimmune disorders |
Sjogren's Syndrome
Sarcoidosis
SLE
Anti–tubular basement membrane antibody-mediated tubulointerstitial nephritis Tubulointerstitial nephritis with uveitis | ||
|
| Balkan endemic nephropathy | ||
| Heavy metal nephropathy | Lead - Gout! - Serum lead levels aren't helpful (most is in bone) - EDTA mobilization testing with 24hr urine lead excretion (>600mcg/24hrs = diagnostic)
Cadmium Mercury | ||
| Hereditary tubulointerstitial nephritis | Medullary cystic disease (type II is associated with hyperuricemia and gout) - Urate Nephropathy (alkaline urate salts deposit into interstitium, causing inflammation -- nephritis)
Mitochondrial disorders | ||
| Infection-related | Direct infiltration or reactive systemic inflammatory response can cause this. Risk factors:
Organisms:
| ||
| Malignancy-related | Mostly multiple myeloma & lymphoproliferative disorders Multiple Myeloma:
Lymphoproliferative Disorders
| ||
| Medication-induced |
| ||
| Secondary Tubulointerstitial Injury | glomerular and vascular disorders | ||
| Urinary Tract Obstruction | Functional or structural - Obstruction & relfux --> inflammation of interstitium --> atrophy |
Management
- Catch early and treat underlying cause (early ones can be reversed)
- Approach:
- Stop drugs
- Removal of exogenous toxins
- Diagnose immunologic, infectious, or malignant disease
- Rule out obstruction
- Treat underlying cause
- Consider immunsuppressants in consultation with nephrologist
GFR Estimation
- Ways to estimate:
- Modification of Diet in Renal Disease (MDRD) study
- Underestimates GFR at higher (normal) values.
- If calculated eGFR is >60 mL/min/1.73m^2 then report as 60.
- Study included patients with CKD with lower muscle mass than general population.
- Underestimates GFR in healthy, low-risk persons with normal/increased muscle mass.
- Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
- Reduced bias associated with MDRD, shown in NHANES study.
- NHANES: median eGFR was 94.5 mL/min/1.73m^2 using CKD-EPI and 85 using MDRD.
- Some patients Stage 3 CKD via MDRD and no CKD by CKD-EPI.
- Reduced bias associated with MDRD, shown in NHANES study.
- Cockcroft-Gault
- Underestimates GFR at higher values.
- Less accurate than MDRD and CKD-EPI?
- 24-hour urine collection - for Creat Clearance.
- Good but inaccurate due to difficulty in collecting 24-hr urine sample.
- Undercollection = inaccurate GFR.
- Radionucleotide kidney clearance scanning
- Very accurate, but more invasive and expensive than eGFR.
- Often used in evaluating live kidney donors.
- Modification of Diet in Renal Disease (MDRD) study
-
CKD Stage GFR level (mL/min/1.73 m2) Stage 1 ≥ 90 Stage 2 60 - 89 Stage 3 30 - 59 Stage 4 15 - 29 Stage 5 < 15
Hyperphosphatemia
In addition to dietary counseling regarding a low phosphate diet, this patient with stage G4/A1 chronic kidney disease (CKD) who now has hyperphosphatemia should begin taking a phosphate binder such as sevelamer. Elevated serum phosphorus levels, particularly exceeding 6.5 mg/dL (2.09 mmol/L), are closely associated with increased mortality. Most patients with severe CKD require oral phosphate binders to be administered with meals. This patient also has known cardiovascular disease and vascular calcification. The Kidney Disease Improving Global Outcomes (KDIGO) guidelines suggest avoiding the use of calcium-containing phosphate binders in patients with known vascular calcification due to the potential for an increase in calcium absorption and worsening calcification of vessel walls. Therefore, a non-calcium–containing phosphate binder such as sevelamer or lanthanum is the preferred agent for this patient. Ferric citrate, another non-calcium–containing phosphorus binder, was recently approved for use in patients receiving dialysis but is not yet approved for patients with non-dialysis CKD.
Although this patient has secondary hyperparathyroidism, administration of calcitriol will increase intestinal absorption of calcium and phosphorus, which will exacerbate the hyperphosphatemia and potentially worsen vascular calcification.
Although administration of oral calcium carbonate will lead to increased absorption of calcium that may treat this patient's mild hypocalcemia and reduce her parathyroid hormone (PTH) levels, it may exacerbate vascular calcium in the setting of severe hyperphosphatemia.
Administration of the calcimimetic cinacalcet will likely decrease this patient's PTH level toward the normal range; however, it will worsen her hypocalcemia and is not an effective treatment for the hyperphosphatemia.
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