eMedicine Specialties > Nephrology > Chronic Kidney Disease
Uremia: Treatment & Medication
Updated: Oct 2, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
The ultimate treatment for uremia is dialysis. Initiate dialysis when signs or symptoms of uremia (eg, nausea, vomiting, volume overload, hyperkalemia, severe acidosis) are present and are not treatable by other medical means. Patients with uremia must have dialysis initiated as soon as symptoms are present, regardless of GFR. For asymptomatic patients, dialysis is generally initiated when their creatinine clearance is 10 mL/min (creatinine level of 8-10 mg/dL) or less or, for diabetic patients, when their creatinine clearance is 15 mL/min (creatinine level of 6 mg/dL). Early referral to a nephrologist for evaluation (when creatinine level is > 3 mg/dL) is essential for patient education and preparation for dialysis or transplantation.
Patients may decide on peritoneal dialysis or hemodialysis, a decision dependent on their preference and level of motivation. Peritoneal dialysis is preferred for patients who are highly motivated, need flexibility in their dialysis schedule, and who may have underlying cardiovascular disease.5 Hemodialysis requires a functioning arterial venous dialysis access and may be accomplished at home or in a center.6 Regardless of whether a patient chooses peritoneal dialysis or hemodialysis, dialysis access must be discussed and placed early. Newer methods of dialysis include daily hemodialysis and nocturnal hemodialysis, the advantages of which include improved volume control, improved cardiovascular disease, improved calcium-phosphate balance, improved dietary parameters, and improved quality of life.
Renal transplantation is the best renal replacement therapy and results in improved survival and quality of life. Transplants from living, related donors are best, but transplants from living, unrelated donors should also be considered. Consider transplantation prior to the need for dialysis because the waiting list for cadaver transplants often exceeds 2-3 years.
- Hyperkalemia: Patients with renal failure associated hyperkalemia of 6.5 mEq/L or greater are candidates for emergent dialysis therapy, particularly if the hyperkalemia is associated with ECG changes (eg, peaked T waves, atrioventricular block, bradycardia). Short-term temporizing measures include intravenous infusion of calcium gluconate to stabilize cardiac membranes, bicarbonate, insulin and glucose administration, or inhaled or intravenous beta-agonists. Nonemergent hyperkalemia can be treated with oral potassium binders (eg, sodium polystyrene sulfonate [Kayexalate]). Correction of acidemia may improve potassium balance. Also, it is imperative to discontinue any medicine that might be contributing to the hyperkalemia, including ACE inhibitors, angiotensin-receptor blockers, beta-blockers, potassium-sparing diuretics, and nonsteroidal anti-inflammatory drugs.
- Anemia: Begin the workup for anemia when the hemoglobin level is less than 11 g/dL or the hematocrit value is less than 33% in premenopausal females and prepubertal patients or when the hemoglobin level is less than 12 g/dL or the hematocrit value is less than 37% in men and postmenopausal women. In patients found to have anemia of chronic kidney disease, it is important to check iron studies and to begin the initial treatment with iron replacement if there is evidence of iron deficiency. The serum ferritin level should be greater than 100 mcg/mL.
- For patients with ESRD and CKD, the goal hemoglobin level should be 11-13 g/dL. There is insufficient evidence to recommend routinely maintaining hemoglobin levels at 13 g/dL or greater in ESA-treated patients, especially because several trials have demonstrated a potential for increased cardiac events in subjects treated to higher hemoglobin levels.7,8
- If the anemia is not corrected, then begin treatment with 1 of 2 subcutaneous erythropoiesis stimulating agents, recombinant human erythropoietin (Epo) or darbepoetin, a unique molecule that stimulates erythropoiesis and has a longer half-life than erythropoietin.
- Initiate iron therapy concurrently with dialysis therapy. Start with one of several intravenous iron preparations as these better absorbed than oral formulations. These can be administered with each dialysis treatment to load the patient with iron or once weekly to maintain iron stores.
- For patients not yet on dialysis, oral iron preparations are used initially. For significant iron deficiency, intravenous iron (InFeD Injection) may be administered slowly (500 mg over 4-6 h) after the administration of a test dose (25 mg).
- Hyperparathyroidism, hypocalcemia, hyperphosphatemia, and renal osteodystrophy: Evaluate and treat secondary hyperparathyroidism, manifested by low calcium levels, high phosphate levels, and low levels of 1,25(OH)2 vitamin D-3, early because it is one of the first manifestations of renal osteodystrophy. Hypocalcemia can be treated with oral calcium carbonate or calcium acetate at a dose of 500 mg to 1 gram orally 3 times a day taken in between meals. If 1,25(OH)2 vitamin D-3 levels are depressed, calcium levels are decreased, and parathyroid levels are elevated (>300), consider initiating oral vitamin D therapy. The dosage of calcitriol is 0.25 mcg orally once daily or 3 times a week, depending on the levels of 1,25(OH)2 vitamin D-3 and PTH.
- When the creatinine clearance falls below 25-30 cc/min, the kidney begins to lose the ability to completely excrete excess amounts of phosphorus. Thus, it is not uncommon for many patients with CKD and ESRD to become hyperphosphatemic. Initial treatment is dietary counseling and modification. If this fails, treatment then consists of administration of oral phosphate binders given with meals. These can include calcium-based formulations, such as calcium carbonate or calcium acetate, or noncalcium-based formulations, such as sevelamer or lanthanum carbonate.
- Acidemia: Acidemia should be treated in patients with a serum bicarbonate level consistently less than 20 mEq/dL. Oral bicarbonate solution or tablets can be used, and most patients will require 0.5-1 mEq/kg of body weight of bicarbonate. Use this therapy cautiously in persons with significant fluid retention and hypertension because of the risk of worsening the fluid retention.
Surgical Care
Surgical referral is necessary for dialysis access placement after the decision regarding dialysis has been made. Renal replacement therapy can be accomplished by hemodialysis, peritoneal dialysis, or transplantation. Referral to an appropriate surgeon (ie, vascular, general, transplant) is made after the modality for renal replacement therapy has been determined.
In general, referral to a vascular surgeon for consideration of dialysis access is initiated by the nephrologist early in the patient's course of renal failure to avoid emergent dialysis access placement. Dialysis access can be conducted through either an arteriovenous fistula for hemodialysis or a peritoneal dialysis catheter for chronic ambulatory peritoneal dialysis or continuous cycling peritoneal dialysis.
- Arteriovenous fistulas are the dialysis access of choice for hemodialysis.
- Avoid arteriovenous Gore-Tex grafts if at all possible because of their poor longevity. Avoid long-term use of tunneled catheters because of the increased risk of infection and poor dialysis adequacy. Avoid subclavian catheters because of their association with increased venous stenosis, thrombosis, or both.
- Peritoneal dialysis access can be accomplished by the placement of a Tenckhoff peritoneal dialysis catheter by either an experienced nephrologist or a surgeon. Direct visualization of the peritoneum is associated with fewer complications and better function of the catheter. Peritoneal dialysis allows patients more control and flexibility with their dialysis treatment regimen.
- Consider any surgery carefully in patients with uremia because of the increased risk for uremic bleeding, cardiovascular events, ARF, respiratory depression, and decreased metabolism of certain drugs. Vasopressin may be considered if uremic bleeding is substantial.
Consultations
Consider consulting a nephrologist as soon as possible in the course of the patient's disease, particularly when renal function test results are only mildly abnormal. Acute hyperkalemia, volume overload, severe acidemia, or a change in mental status, which can progress to stupor or coma, requires emergent consultation with a nephrologist and, possibly, the initiation of dialysis.
Diet
Dietary changes should be made only with the help of a dietitian knowledgeable in renal diet treatment, particularly in patients who have not yet started dialysis therapy.
- A low-protein diet has been advocated for persons with mild-to-moderate renal failure, although this matter remains controversial. Low-protein diets may alleviate some of the symptoms of uremia, such as nausea; however, data regarding the renoprotective effect of low-protein diets are conflicting. The MDRD study analyzed 585 patients with nondiabetic chronic renal disease and a mean GFR of 39 mL/min. Patients were randomized to protein intakes of either 1.1 g/kg/d or 0.7 g/kg/d. Despite good compliance, there appeared to be little overall benefit with the low-protein diet. Also, low-protein diets can cause the patient to become malnourished, which has been associated with higher mortality upon the initiation of dialysis.
- On the other hand, in an analysis of studies comparing the consumption of different protein levels by nondiabetic adults with moderate to severe kidney failure, Fouque and Laville concluded that a low-protein diet can lower rate of "renal death" (which they defined as kidney transplantation, the need to begin dialysis, or the death of a patient) by 32%.9 Incorporating results from 2000 patients, including 1002 who had consumed a reduced-protein diet, the authors found that 113 renal deaths had occurred in the low-protein group and 168 in the higher-protein group. However, the authors stated that they were unable to confirm through their analysis an optimal protein intake level for persons with renal failure.
- Current recommendations for a low-protein diet prior to the initiation of dialysis are 0.8-1 gram of protein/kg of weight, with an additional gram of protein added for each gram of protein lost in the urine (for patients with nephrotic syndrome).
- Patients with advanced uremia or malnutrition are not candidates for a low-protein diet.
- Patients with CRF should be on a low-potassium (2-3 g/d), low-phosphate (2 g/d), and low-sodium (2 g/d) diet.
Activity
Activity for patients with uremia is self-restricted based on their level of fatigue.
- Early treatment of anemia with iron and EPO improves the quality of life and energy levels even before the patient needs dialysis.
- Bleeding secondary to uremia may occur; dangerous activities may need to be restricted and potential bleeding sites assessed in the event of a fall (eg, for a subdural hematoma).
Medication
Usually, medications used for uremia are indicated to treat associated metabolic and electrolyte abnormalities, such as anemia, hyperkalemia, hypocalcemia, hyperparathyroidism, and iron deficiency. Medication selection and dosage depend on the patient's clinical state, which may change with the acute clinical setting. Dialysis is the primary treatment for uremia, but medications can effectively treat some of the associated symptoms and clinical abnormalities (eg, anemia, hypocalcemia).
Colony-stimulating factors
Increase reticulocyte count, hematocrit value, and hemoglobin levels.
Epoetin alfa (Epogen, Procrit)
Purified glycoprotein produced from mammalian cells modified with gene coding for human EPO. Biological activity mimics human urinary EPO, which stimulates division and differentiation of committed erythroid progenitor cells and induces release of reticulocytes from bone marrow into the blood stream. Indicated for treatment of anemia associated with CRF or renal insufficiency.
Adult
50-150 U/kg IV/SC 3 times/wk
Pediatric
Not established
None reported
Documented hypersensitivity; uncontrolled hypertension
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in porphyria, hypertension, ischemic vascular disease, or history of seizures; decrease dose if hematocrit value increases > 4 U in any 2-wk period
Calcium supplements
Used to correct hypocalcemia and improve symptoms associated with renal osteodystrophy. Also may be used to bind phosphate in patients with hyperphosphatemia.
Calcium carbonate (Caltrate, Os-Cal 500, Alka-Mints, Tums)
Indicated for treatment of hyperphosphatemia secondary to CRF. Effectively normalizes phosphate concentrations in dialysis patients. Combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. Marketed in a variety of dosage forms and is relatively inexpensive.
Adult
1-2 g PO divided bid/qid taken with meals
Pediatric
45-65 mg/kg/d PO divided qid taken with meals
May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; large intakes of dietary fiber may decrease calcium absorption and levels; enhances effects/toxicity of digitalis
Documented hypersensitivity; renal calculi, hypercalcemia, hypophosphatemia, renal or cardiac disease, patients with digitalis toxicity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypercalcemia or hypercalciuria may occur at therapeutic doses
Calcium acetate (PhosLo, Calphron)
Indicated for treatment of hyperphosphatemia secondary to CRF. Effectively normalizes phosphate concentrations in dialysis patients. Combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces.
Adult
2 tabs PO tid with meals; titrate up until serum phosphate is 6 mg/dL, as long as hypercalcemia does not develop; may require as many as 4 tab PO tid
Pediatric
Not established
May increase effect of quinidine; may decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels; enhances effects/toxicity of digitalis
Documented hypersensitivity; hypercalcemia, hypophosphatemia, renal calculi
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypercalcemia or hypercalciuria may occur at therapeutic doses
Vitamins
Essential for normal metabolism of proteins, carbohydrates, and fats and normal DNA synthesis. Used in the treatment of hyperparathyroidism, vitamin D deficiency, and renal osteodystrophy.
Paricalcitol (Zemplar)
For treatment of secondary hyperparathyroidism in ESRD. Reduces PTH levels, stimulates calcium and phosphorous absorption, and stimulates bone mineralization.
Adult
0.04-0.1 mcg/kg IV bolus 3 times/wk; adjust dose based on PTH levels
Pediatric
<5 years: Not established
5-19 years: 0.04-0.08 mcg/kg IV 3 times/wk; adjust dose based on PTH levels
Do not use phosphate or vitamin D-related compounds concomitantly with paricalcitol; caution if administered with digoxin (digitalis toxicity is potentiated by hypercalcemia)
Documented hypersensitivity; hypercalcemia; vitamin D toxicity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in breastfeeding; adverse effects include GI tract distress, dry mouth, lightheadedness, edema, chills, or fever
Calcitriol (Rocaltrol)
Two known sites of action are intestine and bone. Other evidence indicates that it also acts on kidneys and parathyroid gland. Vitamin D-3 must be converted to calcitriol in liver and kidneys before it is fully active on its target tissues. Some evidence suggests that uremic patients have vitamin D–resistant state because of a failure of their kidney to metabolically activate vitamin D-3 to calcitriol, which increases calcium levels by promoting absorption of calcium in intestines and retention in kidneys.
Adult
0.25 mcg PO qd, increase at 4- to 8-wk intervals by 0.25 mcg prn
Pediatric
Initial: 15 ng/kg/d PO
Maintenance: 5-40 ng/kg/d PO
Cholestyramine and colestipol decrease absorption; magnesium-containing antacids and thiazide diuretics can increase effects
Documented hypersensitivity; hypercalcemia; malabsorption syndrome
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adequate response depends on adequate dietary calcium intake; maintain adequate fluid intake
Iron salts
Used to correct iron deficiency symptoms.
Ferrous sulfate (Feosol)
A nutritionally essential inorganic substance necessary for hemoglobin formation and oxidative processes of living tissue. Effectively treats iron deficiency anemia.
Adult
325 mg PO qd, increase to tid prn
Pediatric
<15 kg: 5 mg/kg/d PO
15-30 kg: Half of adult dose
>30 kg: Administer as in adults
Absorption is enhanced by ascorbic acid; interferes with tetracycline absorption; food and antacids impair absorption
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
GI upset; iron toxicity observed with ingestion of large amounts and can be fatal, especially in children; parenteral (IV) administration may cause several reactions, including headaches, malaise, fever, generalized lymphadenopathy, arthralgia, and urticaria; can cause severe anaphylaxis; others include phlebitis at infusion site
Antidotes
Used to reduce serum potassium levels.
Sodium polystyrene sulfonate (Kayexalate)
Exchanges sodium for potassium, binds it in the gut (primarily in the large intestine), and decreases total body potassium. PO onset of action ranges from 2-12 h and is longer when PR.
Adult
25-50 g PO q6h in 25-50 mL sorbitol
25-50 g PR q6h in 25-50 mL sorbitol as retention enema
Pediatric
1.0 g/kg PO q6h in sorbitol
2.0 g/kg PR q6h in sorbitol as retention enema
Systemic alkalosis may occur if administered concurrently with magnesium hydroxide, aluminum carbonate or similar antacids, and laxatives
Documented hypersensitivity; hypernatremia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients who can be adversely affected by a small increase in sodium loads (eg, those with severe hypertension, severe congestive heart failure, and marked edema); constipation with the possibility of fecal impaction may occur; treat constipation with 10-20 mL of 70% sorbitol q2h or prn to produce at least 1-2 watery stools qd
Antidiabetic agents
Stimulate cellular uptake of potassium.
Insulin (Humulin R, Novolin R)
Stimulates cellular uptake of potassium within 20-30 min. Administer glucose along with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently.
Adult
10 U IV and 50 mL D50W bolus or 500 mL D10W over 1 h
Pediatric
0.5-1.0 g/kg (as D50W or equivalent) IV followed by 1 U of regular insulin per 3 g glucose
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hyperthyroidism may increase renal clearance of insulin and patient may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments may be necessary in patients diagnosed with renal or hepatic dysfunction
Phosphate binders
Used to bind phosphate when calcium carbonate or acetate cannot be used because of a high serum calcium level.
Sevelamer (Renagel)
Cationic polymer that binds intestinal phosphate, which is excreted in the feces. Not absorbed and does not contain calcium or aluminum ions. Binding of bile salts may also occur, which may result in lowered low-density lipoprotein cholesterol levels.
Adult
800-1600 mg PO with each meal
Pediatric
Not established
May reduce absorption of coadministered drugs
Documented hypersensitivity; bowel obstruction, hypophosphatemia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with dysphagia, severe GI motility disorders, or swallowing disorders; can cause hypophosphatemia in patients with low or normal serum phosphate levels; when changes in absorption of PO medications may have clinical consequences (eg, antiseizure or antiarrhythmic drugs), medications should be taken 1 h before or 3 h after a dose of sevelamer
Lanthanum carbonate (Fosrenol)
Noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with end-stage renal disease. Directly binds dietary phosphorus in upper GI tract, thereby inhibiting phosphorus absorption.
Adult
Initial: 250-500 mg PO tid pc (chewable tabs); adjust dose q2-3wk to target serum phosphorus level
Maintenance: 500-1000 mg PO tid pc
Pediatric
Not established
Drugs known to interact with antacids (eg, alendronate, amprenavir, ciprofloxacin, itraconazole, tetracycline, thyroid hormones) should not be administered within 2 h
Documented hypersensitivity; bowel obstruction; hypophosphatemia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Deposited into developing bone, including growth plate (long-term effects unknown); common adverse effects typically diminish over time but include headache, abdominal pain, nausea, diarrhea, constipation, and vomiting; in clinical trials, dialysis graft occlusion occurred more frequently than with placebo; caution with GI motility diseases (eg, Crohn disease, ulcerative colitis) or recent GI surgery
More on Uremia |
| Overview: Uremia |
| Differential Diagnoses & Workup: Uremia |
 Treatment & Medication: Uremia |
| Follow-up: Uremia |
| References |
| Further Reading |
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References
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Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med. Jul 31 2003;349(5):446-56. [Medline].
Sprague SM, Llach F, Amdahl M, Taccetta C, Batlle D. Paricalcitol versus calcitriol in the treatment of secondary hyperparathyroidism. Kidney Int. Apr 2003;63(4):1483-90. [Medline].
Muscaritoli M, Molfino A, Bollea MR, et al. Malnutrition and wasting in renal disease. Curr Opin Clin Nutr Metab Care. Jul 2009;12(4):378-83. [Medline].
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Fouque D, Laville M. Low protein diets for chronic kidney disease in non diabetic adults. Cochrane Database Syst Rev. Jul 8 2009;CD001892. [Medline].
Baigent C, Burbury K, Wheeler D. Premature cardiovascular disease in chronic renal failure. Lancet. Jul 8 2000;356(9224):147-52. [Medline].
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Lim VS, Kopple JD. Protein metabolism in patients with chronic renal failure: role of uremia and dialysis. Kidney Int. Jul 2000;58(1):1-10. [Medline].
May RC, Mitch WE. Pathophysiology of uremia. In: Brenner BM, ed. Brenner & Rector's The Kidney. Vol 2. 5th ed. Philadelphia, Pa: WB Saunders; 1996:2148-69.
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Further Reading
Clinical guidelines:
Diagnosis and management of adults with chronic kidney disease. Michigan Quality Improvement Consortium - Professional Association. 2006 Nov (revised 2008 Nov). 1 page. NGC:007053
(1) KDOQI clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease. (2) 2007 update of hemoglobin target. National Kidney Foundation - Disease Specific Society. 1997 (updated 2006 May; addendum released 2007 Sep). Original guideline: 145 pages; addendum: 60 pages. NGC:006019
NKF-KDOQI clinical practice guidelines for peritoneal dialysis adequacy: update 2006. National Kidney Foundation - Disease Specific Society. 1997 (updated 2006 Jul). 32 pages. NGC:005330
Clinical trials:
Analysis of Calcium Balance in Chronic Kidney Disease
Dietary Intervention and Exercise Training (DIET) in Moderate to Severe Chronic Kidney Disease
Low Phosphate Diets in Patients With Early Stages of Chronic Kidney Disease
Phase 2 Study of FG-4592 in Subjects With Anemia and Chronic Kidney Disease Not Requiring Dialysis
Safety Study of CTA018 Injection to Treat Stage 5 Chronic Kidney Disease
Study to Assess Darbepoetin Alfa Dosing for the Correction of Anemia in Pediatric Subjects With Chronic Kidney Disease
Keywords
uremia, chronic renal failure, end-stage renal disease, ESRD, CRF, end-stage renal failure, renal failure, RF, kidney failure, chronic kidney failure, end-stage kidney disease, end-stage kidney failure, anemia, uremic syndrome, chronic kidney disease, CKD, azotemia, uremic pericarditis, acidosis, hyperkalemia, uremic endocrine abnormality, uremic heart disease, uremic anorexia, uremic encephalopathy, primary glomerular disease, glomerulonephritis
focal segmental glomerulosclerosis, FSGS, rapidly progressive glomerulonephritis, systemic glomerular disorder, diabetes, lupus, amyloidosis, Goodpasture disease, Goodpasture's disease, thrombotic thrombocytopenicpurpura, TTP, hemolytic uremic syndrome, HUS, hypertension, glomerulonephritis, interstitial disease, cystitis, immunoglobulin A nephropathy, IgA nephropathy, glomerulonephropathies, glomerulonephropathy
