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• W2017773190 abstract "Renal disease is commonly encountered by primary care physicians during their day-to-day visits with patients. Common renal disorders include hypertension, proteinuria, kidney stones, and chronic kidney disease. Despite their prevalence, many physicians may be unfamiliar with the diagnosis and initial treatment of these common renal disorders. Early recognition and intervention are important in slowing the progression of chronic kidney disease and preventing its complications. The evidence-based pearls in this article will help primary care physicians avoid common pitfalls in the recognition and treatment of such disorders and guide their decision to refer their patients to a specialist. Renal disease is commonly encountered by primary care physicians during their day-to-day visits with patients. Common renal disorders include hypertension, proteinuria, kidney stones, and chronic kidney disease. Despite their prevalence, many physicians may be unfamiliar with the diagnosis and initial treatment of these common renal disorders. Early recognition and intervention are important in slowing the progression of chronic kidney disease and preventing its complications. The evidence-based pearls in this article will help primary care physicians avoid common pitfalls in the recognition and treatment of such disorders and guide their decision to refer their patients to a specialist. Chronic kidney disease (CKD) is a widespread public health problem with substantial morbidity and mortality. Outcomes associated with CKD are progression to kidney failure, cardiovascular disease, and premature death. Learning to recognize CKD in its earliest stage and understanding what measures to undertake to prevent its progression and associated complications are important goals developed by the Kidney Disease: Improving Global Outcomes (KDIGO) initiative.1Levey AS Eckardt KU Tsukamoto Y et al.Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).Kidney Int. 2005; 67: 2089-2100Crossref PubMed Scopus (2528) Google Scholar The evaluation of difficult-to-treat hypertension and kidney stones are additional skills that primary care physicians will need to acquire. The evidence-based pearls in this article will help primary care physicians understand these concepts and avoid common pitfalls in the recognition and treatment of such disorders and guide their decision to refer their patients to a specialist. 1.A “Normal” Serum Creatinine Level May Not Be Normal.Normal creatinine values may vary among different laboratories, and some patients with serum creatinine levels within the “normal” range may have substantial reduction in kidney function. For example, a 66-year-old man with a serum creatinine level of 1.4 mg/dL (to convert to μmol/L, multiply by 88.4) would have an estimated glomerular filtration rate (GFR) of 54 mL/min per 1.73 m2. This perceived “normal” serum creatinine value actually corresponds to stage 3 CKD.1Levey AS Eckardt KU Tsukamoto Y et al.Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).Kidney Int. 2005; 67: 2089-2100Crossref PubMed Scopus (2528) Google Scholar Likewise, the rate of increase or trend of serum creatinine levels can also indicate CKD. For example, a 66-year-old man with a serum creatinine level of 0.8 mg/dL and an estimated GFR of 103 mL/min per 1.73 m2 would have an estimated GFR of less than 64 mL/min per 1.73 m2 should the serum creatinine level stabilize at 1.2 mg/dL. This would represent at least a 40% reduction in GFR. Estimates of GFR can only be based on steady-state serum creatinine values and cannot be used to accurately estimate GFR when it is changing. A rapid increase in the serum creatinine level from 0.8 to 1.2 mg/dL within 8 hours could reflect a GFR approaching zero in a patient with acute renal failure. The interpretation of serum creatinine level also depends on muscle mass, age, sex, height, and limb amputation. A patient with an amputation and a high-normal creatinine level may actually have advanced CKD. Commonly used GFR estimation equations, such as the Modification of Diet in Renal Disease calculator (www.mdrd.com), have not been validated in patients with normal GFR and in fact may underestimate actual GFR in healthy people.2Fadem SZ MDRD GFR Calculator (With SI Units): Web site. 4 variable MDRD study equation using serum creatinine, age, race, gender.http://www.mdrd.com/Google Scholar The take-home message is that recognition of CKD is important in order to identify and treat reversible causes of renal disease, slow the progression and avoid the complications of renal disease, and identify patients who may need dialysis or a renal transplant.1Levey AS Eckardt KU Tsukamoto Y et al.Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).Kidney Int. 2005; 67: 2089-2100Crossref PubMed Scopus (2528) Google Scholar2.Know the Medications That Spuriously Elevate the Serum Creatinine Level.In a number of scenarios, the serum creatinine level can increase without reflecting a change in the actual GFR. The antibiotic trimethoprim-sulfamethoxazole and the H2-blocker cimetidine are 2 commonly used drugs that decrease the secretion of creatinine. This can result in a self-limited and reversible increase in the serum creatinine level of as much as 0.4 to 0.5 mg/dL (depending on baseline serum creatinine level). Famotidine and ranitidine can likewise cause an increase but to a lesser degree. The antibiotic cefoxitin can spuriously increase the serum creatinine level by interfering with the colorimetric assay used to measure serum creatinine levels.3Stevens L Perrone RD Drugs that elevate the serum creatinine concentration UpToDate Online.http://uptodateonline.com/online/content/topic.do?topicKey=fldlytes/32725&selectedTitle=2∼150&source=search_resultGoogle Scholar In both instances, the blood urea nitrogen (BUN) typically does not change. As such, an increase in creatinine level suggests a true decrease in GFR only if accompanied by a corresponding increase in BUN levels.3.Patients With Decreased GFR or Proteinuria Should Be Evaluated to Determine the Cause; Positive Urine Dipstick Test Results for Protein Should Be Followed Up With a Spot Urine Protein to Urine Creatinine Ratio.Chronic kidney disease is defined as a kidney abnormality that persists for more than 3 months. Persons with a normal GFR may have CKD if they have persistent proteinuria or hematuria of renal origin. Despite the difficulty associated with accurate assessment of near-normal GFR, most would agree that a persistent GFR of less than 60 mL/min per 1.73 m2 would signify CKD. Proteinuria is initially detected by the urine dipstick test, which reflects the concentration of albumin in the urine. Because variations in urine flow and concentration can affect the semiquantitative dipstick determination, a quantitative estimation of proteinuria is required.The preferred method for quantitative estimation of protein excretion is the spot urine protein to creatinine ratio because it is accurate and more convenient than a 24-hour urine collection.4Kannel WB Stampfer MJ Castelli WP Verter J The prognostic significance of proteinuria: the Framingham study.Am Heart J. 1984; 108: 1347-1352Abstract Full Text PDF PubMed Scopus (364) Google Scholar, 5K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification, Part 5: evaluation of laboratory measurements for clinical assessment of kidney disease guideline 5. assessment of proteinuria. NKF K/DOQI Web site.http://www.kidney.org/Professionals/Kdoqi/guidelines_ckd/p5_lab_g5.htmGoogle Scholar, 6Ginsberg JM Chang BS Matarese RA Garella S Use of single voided urine samples to estimate quantitative proteinuria.N Engl J Med. 1983; 309: 1543-1546Crossref PubMed Scopus (625) Google Scholar, 7Schwab SJ Christensen RL Dougherty K Klahr S Quantitation of proteinuria by the use of protein-to-creatinine ratios in single urine samples.Arch Intern Med. 1987; 147: 943-944Crossref PubMed Scopus (226) Google Scholar In patients at risk of proteinuria (eg, patients with diabetes), a spot urine albumin to creatinine ratio is helpful for detecting microalbuminuria, thereby guiding further therapy. Patients with diabetes who have microalbuminuria may be at higher risk of developing diabetic nephropathy. In a patient with a urine protein to creatinine ratio of 1 or more, the risk of progression of CKD is higher. In fact, any patient with an elevated ratio (≥1) should be evaluated for causes of glomerular disease, including diabetes, collagen vascular disease (eg, systemic lupus erythematosus), malignancy (eg, multiple myeloma), infections (eg, human immunodeficiency virus infection, syphilis, hepatitis B and C), and use of medications such as nonsteroidal anti-inflammatory drugs (NSAIDs).8Warren GV Korbet SM Schwartz MM Lewis EJ Minimal change glomerulopathy associated with nonsteroidal antiinflammatory drugs.Am J Kidney Dis. 1989 Feb; 13: 127-130PubMed Scopus (75) Google Scholar Solid tumors may also be associated with glomerular disease (membranous glomerulopathy), but such tumors are generally either already known or readily detectable by age-, risk-, and sex-appropriate cancer screening.9Burstein DM Korbet SM Schwartz MM Membranous glomerulonephritis and malignancy.Am J Kidney Dis. 1993; 22: 5-10PubMed Scopus (150) Google Scholar, 10Brueggemeyer CD Ramirez G Membranous nephropathy: a concern for malignancy.Am J Kidney Dis. 1987; 9: 23-26PubMed Scopus (45) Google Scholar Patients with a high degree of proteinuria or active urinary sediment, especially in the setting of deterioration in kidney function, should be referred to a nephrologist for further evaluation and treatment. A lower degree of proteinuria in association with CKD (unmodified by antiangiotensin or antialdosterone agents) suggests a nonglomerular etiology (Table). This Table should not be considered to be all inclusive; instead, it provides a conceptual framework for approaching the identification of the numerous causes of nonglomerular CKD. Preglomerular, intrarenal, and postrenal causes may be associated with long-term reductions in renal function and lower degrees of proteinuria. The key to the diagnostic assessment of patients with these conditions includes, most importantly, a careful history and physical examination, followed by renal Doppler ultrasonography to detect renal artery stenosis, obstruction, and/or cysts.TABLECauses of Low Proteinuric CKDaACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin II receptor blocker; CKD = chronic kidney disease; NSAID = nonsteroidal anti-inflammatory drug.Anatomic locationBasis of diagnosisInterventionPreglomerular Cardiomyopathy (cardiorenal syndrome)History, physical examination findingsOptimize heart failure treatment Hepatic cirrhosisHistory, physical examination findingsPrevent further kidney damage due to overdiuresis, exposure to NSAIDs, or large-volume paracentesis Renal artery stenosisRisk assessment for atherosclerotic disease; fluctuating renal function with sensitivity to ACEI, ARB, or volume depletion; difficult-to-control hypertension; findings on Doppler ultrasonographyOptimize lipid control in patients with atherosclerotic disease and consider vascular intervention (eg, percutaneous arterial intervention) Nephrosclerosis and nephroatherosclerosisHistory of prolonged poorly controlled hypertensionControl blood pressureIntrarenal nonglomerular Polycystic kidney diseaseFamily history, palpable kidneys, renal and hepatic ultrasonographic findingsInitiate antiangiotensin agents and ensure adequate hydration Previous acute kidney injury with incomplete recoveryHistory of kidney failure, previous need for dialysis, review of previous laboratory test results if availablePrevent recurrent injury Long-term exposure to potentially nephrotoxic agentsHistory of analgesic or NS AID use, lithium therapy, herb use, cocaine use, lead exposure, risk factors for milk-alkali syndrome, previous exposure to a phosphate-based bowel preparation for colonoscopy (see text, section 7)If possible, avoid further exposure Recurrent renal stone diseaseHistory of multiple episodes of nephrolithiasis, findings on 24-hr urine stone risk panel. Assess for primary hyperparathyroidismDevelop a plan to reduce stone risk on the basis of the stone risk assessment (see text, section 10)Postrenal Partial or past obstructionHistory of urological symptoms (prostatism), problems, or procedures; findings on ultrasonography. Assess for prostate cancer, if applicableRelieve obstruction if present and consult with a urologista ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin II receptor blocker; CKD = chronic kidney disease; NSAID = nonsteroidal anti-inflammatory drug. Open table in a new tab 4.In Patients With Early-Stage CKD, Periodic Evaluation and Intervention Are Appropriate to Slow the Progression of Renal Disease and Avoid Its Complications.In patients with CKD, it is imperative to slow the rate of disease progression. Nephrotoxic drugs, such as NSAIDs, aminoglycoside antibiotics, and radiocontrast agents, should be used with caution or avoided completely. Systemic blood pressure should be monitored frequently and controlled with a goal blood pressure of less than 130/80 mm Hg. A lower blood pressure may be desirable in patients with proteinuric CKD. A spot urine protein to creatinine ratio should be obtained periodically, with a ratio of 1 or more suggesting a higher risk of CKD progression.Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) may slow the progression of CKD, especially in patients with proteinuria. In addition to lowering systemic blood pressure, ACEIs and ARBs also lower glomerular capillary blood pressure and protein filtration, which may contribute to their beneficial effect in slowing progression. They may also help reduce angiotensin II-mediated cell proliferation and fibrosis.11K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification, part 4: definition and classification of stages of chronic kidney disease guideline 2. evaluation and treatment. NKF K/DOQI Web Site.http://www.kidney.org/Professionals/Kdoqi/guidelines_ckd/p4_class_g2.htmGoogle Scholar Combination therapy with an ACEI and ARB may have a greater antiproteinuric effect than either drug alone, but patients should be monitored carefully for increases in serum creatinine and potassium levels.11K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification, part 4: definition and classification of stages of chronic kidney disease guideline 2. evaluation and treatment. NKF K/DOQI Web Site.http://www.kidney.org/Professionals/Kdoqi/guidelines_ckd/p4_class_g2.htmGoogle Scholar, 12Wolf G Ritz E Combination therapy with ACE inhibitors and angiotensin II receptor blockers to halt progression of chronic renal disease: pathophysiology and indications.Kidney Int. 2005; 67: 799-812Crossref PubMed Scopus (257) Google Scholar Patients with progressive CKD are at risk of renal osteodystrophy. Phosphorus, calcium, and parathyroid hormone levels should be monitored closely in all patients with stage 3 to 4 CKD. Abnormalities in these values may indicate the need for dietary phosphate restriction, administration of oral phosphate binders, and/or the administration of vitamin D.Patients with CKD also have an increased risk of cardiovascular complications, including myocardial infarction.13Douglas K O'Malley PG Jackson JL Meta-analysis: the effect of statins on albuminuria.Ann Intern Med. 2006; 145: 117-124Crossref PubMed Scopus (223) Google Scholar Aspirin (eg, 81 mg/d) and aggressive lipid-lowering strategies should be used, including 3-hydroxy-3-methylglutaryl (HMG) coenzyme A reductase inhibitors or statins, with a goal low-density lipoprotein cholesterol (LDL-C) level of 100 mg/dL or less (to convert to mmol/L, multiply by 0.0259). In patients with CKD and established coronary artery disease, some physicians recommend a goal LDL-C level of 70 mg/dL or less. Recently, several studies have suggested that statins may have the additional benefit of reducing proteinuria.4Kannel WB Stampfer MJ Castelli WP Verter J The prognostic significance of proteinuria: the Framingham study.Am Heart J. 1984; 108: 1347-1352Abstract Full Text PDF PubMed Scopus (364) Google Scholar, 13Douglas K O'Malley PG Jackson JL Meta-analysis: the effect of statins on albuminuria.Ann Intern Med. 2006; 145: 117-124Crossref PubMed Scopus (223) Google Scholar More studies are needed to determine whether tighter control of LDL-C levels translates into reduction of cardiovascular events or progression to end-stage renal disease.Early referral to a nephrologist should be considered if CKD progresses or if the patient has uncontrolled complications, including nephritic-range proteinuria, uncontrolled blood pressure, uncontrolled secondary hyperparathyroidism, or active urine sediment. Consultation and/or comanagement with a kidney disease care team is advisable for patients with stage 3 CKD (GFR, 30-59 mL/min/1.73 m2). All patients with a GFR of less than 30 mL/min per 1.73 m2 (stages 4-5) should be referred to a nephrologist.9Burstein DM Korbet SM Schwartz MM Membranous glomerulonephritis and malignancy.Am J Kidney Dis. 1993; 22: 5-10PubMed Scopus (150) Google Scholar5.Do Not Automatically Discontinue an ACEI or ARB Solely Because of a Small Increase in the Serum Creatinine or Potassium Level.Two important drugs in the treatment of patients with CKD are ACEIs and ARBs. In management of proteinuric kidney diseases, ACEIs or ARBs are used not only to optimize blood pressure control (Joint National Commission VII) but can be titrated up in patients with proteinuria. They are also the drugs of choice to prevent progression of proteinuric CKD.12Wolf G Ritz E Combination therapy with ACE inhibitors and angiotensin II receptor blockers to halt progression of chronic renal disease: pathophysiology and indications.Kidney Int. 2005; 67: 799-812Crossref PubMed Scopus (257) Google Scholar, 14K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification, part 7: stratification of risk for progression of kidney disease and development of cardiovascular disease guideline 13. Factors associated with loss of kidney function in chronic kidney disease. NKF K/DOQI Web Site.http://www.kidney.org/Professionals/Kdoqi/guidelines_ckd/p7_risk_g13.htmGoogle Scholar, 15Kunz R Friedrich C Wolbers M Mann JF Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease.Ann Intern Med. 2008 Jan 1; 148 (Epub 2007 Nov 5.): 30-48Crossref PubMed Scopus (603) Google Scholar Patients who begin taking or have a dose increase in ACEIs or ARBs may experience an increase in the serum creatinine level. Although an increase of 20% to 30% is acceptable,16Bakris GL Weir MR Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern?.Arch Intern Med. 2000; 160: 685-693Crossref PubMed Google Scholar it is important to confirm that the serum creatinine level stabilizes at the higher value and does not continue to increase. Also, an increase in serum potassium levels is sometimes seen in patients who are taking ACEIs or ARBs. A serum potassium level of up to 5.5 mEq/L (to convert to mmol/L, multiply by 1.0) is acceptable as long as it is stable and as long as the patient is aware of the need for dietary potassium restriction and will not be exposed to additional medications, such as spironolactone, that may exacerbate hyperkalemia. Follow-up serum creatinine and potassium levels should be ordered within 1 week. In patients with an increase in creatinine level of more than 20% to 30% or in those with uncontrollable hyperkalemia, the ACEI or ARB should be discontinued or titrated to a lower dose. Frequent monitoring is necessary. Furthermore, diuretics that work with reduced GFR, such as furosemide or metolazone, are useful agents in the treatment of hypertension and hyperkalemia in CKD. However, it is important to note that volume depletion may make a patient more susceptible to an ACEI- or ARB-induced increase in the serum creatinine level.6.Anemia in Patients With CKD Should Be Treated With Erythrocyte-Stimulating Agents Such as Recombinant Human Erythropoietin But Should Not Be Overtreated.In patients with CKD, anemia has been associated with fatigue, reduced exercise tolerance, dyspnea, left ventricular hypertrophy, left ventricular systolic dysfunction, and an increased risk of cardiovascular events (stroke and myocardial infarction).17Levin A Thompson CR Ethier J et al.Left ventricular mass index increase in early renal disease: impact of decline in hemoglobin.Am J Kidney Dis. 1999; 34: 125-134Abstract Full Text Full Text PDF PubMed Scopus (749) Google Scholar, 18K/DOQI clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease: 2007 update of hemoglobin target.Am J Kidney Dis. 2007; 50: 471-530Abstract Full Text Full Text PDF PubMed Scopus (629) Google Scholar As such, the National Kidney Foundation Dialysis Outcomes Quality Initiative (K/DOQI) guideline for the treatment of anemia of CKD recommends that the hemoglobin target should be between 11 and 12 g/dL (to convert to g/L, multiply by 10) and should not exceed 13 g/dL.18K/DOQI clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease: 2007 update of hemoglobin target.Am J Kidney Dis. 2007; 50: 471-530Abstract Full Text Full Text PDF PubMed Scopus (629) Google Scholar Erythropoietin should be discontinued in patients with a hemoglobin level of 13 g/dL. In a number of well-publicized articles, patients taking erythropoietin who were corrected to normal or near-normal hemoglobin levels were at higher risk of cerebrovascular events, thrombosis, and hypertension.18K/DOQI clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease: 2007 update of hemoglobin target.Am J Kidney Dis. 2007; 50: 471-530Abstract Full Text Full Text PDF PubMed Scopus (629) Google Scholar, 19Phrommintikul A Haas SJ Elsik M Krum H Mortality and target haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin: a meta-analysis.Lancet. 2007; 369: 381-388Abstract Full Text Full Text PDF PubMed Scopus (539) Google Scholar, 20Drüeke TB Locatelli F Clyne N CREATE Investigators et al.Normalization of hemoglobin level in patients with chronic kidney disease and anemia.N Engl J Med. 2006; 355: 2071-2084Crossref PubMed Scopus (1785) Google Scholar, 21Singh AK Szczech L Tang KL CHOIR Investigators et al.Correction of anemia with epoetin alfa in chronic kidney disease.N Engl J Med. 2006; 355: 2085-2098Crossref PubMed Scopus (2280) Google Scholar All patients with anemia should be evaluated for other reversible causes, including vitamin deficiencies and iron deficiency. Routine evaluation would include a reticulocyte count and measurement of serum vitamin B12 and folate, serum iron, ferritin, and total iron-binding capacity. Patients (especially males and nonmenstruating females) with iron deficiency should undergo a gastrointestinal evaluation with endoscopy and colonoscopy. Iron deficiency must be corrected if erythrocyte-stimulating agents are to be effective.7.Phosphate-Containing Bowel Preparations Should Be Used With Caution.Although sodium phosphate bowel preparation agents are effective and more convenient than other agents on the market, several recent studies have suggested that they can cause acute phosphate nephropathy, leading to acute renal failure or worsening of CKD.22Fine A Patterson J Severe hyperphosphatemia following phosphate administration for bowel preparation in patients with renal failure: two cases and a review of the literature.Am J Kidney Dis. 1997; 29: 103-105Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 23Vukasin P Weston LA Beart RW Oral Fleet Phospho-Soda laxative-induced hyperphosphatemia and hypocalcemic tetany in an adult: report of a case.Dis Colon Rectum. 1997; 40: 497-499Crossref PubMed Scopus (81) Google Scholar, 24Ullah N Yeh R Ehrinpreis M Fatal hyperphosphatemia from a phosphosoda bowel preparation.J Clin Gastroenterol. 2002; 34: 457-458Crossref PubMed Scopus (69) Google Scholar A 2005 study reported 21 cases of acute phosphate nephropathy in patients who had undergone a recent colonoscopy and who had taken a sodium phosphate bowel preparation.25Markowitz GS Stokes MB Radhakrishnan J D'Agati VD Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure.J Am Soc Nephrol. 2005 Nov; 16 (Epub 2005 Sep 28.): 3389-3396Crossref PubMed Scopus (325) Google Scholar Although the pathophysiology was not fully understood, it was thought to be secondary to substantial fluid shifts and electrolyte changes. On the basis of their case evaluation, the authors of this study speculated that potential etiologic factors included inadequate hydration, increased patient age, a history of hypertension, and current use of an ACEI or ARB. Subsequently, several professional societies have developed guidelines for the use of sodium phosphate bowel preparations.26Makkar R Shen B What are the caveats to using sodium phosphate agents for bowel preparation?.Cleve Clin J Med. 2008; 75: 173-176Crossref PubMed Scopus (4) Google Scholar, 27Wexner SD Beck DE Baron TH American Society of Colon and Rectal Surgeons American Society for Gastrointestinal Endoscopy Society of American Gastrointestinal and Endoscopic Surgeons et al.A consensus document on bowel preparation before colonoscopy: prepared by a task force from the American Society of Colon and Rectal Surgeons (ASCRS), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES).Gastrointest Endosc. 2006; 63: 894-909Abstract Full Text Full Text PDF PubMed Scopus (282) Google Scholar In addition to the potential etiologic factors identified in the 2005 study,25Markowitz GS Stokes MB Radhakrishnan J D'Agati VD Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure.J Am Soc Nephrol. 2005 Nov; 16 (Epub 2005 Sep 28.): 3389-3396Crossref PubMed Scopus (325) Google Scholar patients with CKD or chronic heart failure and those taking NSAIDs or diuretics would also appear to be at higher risk of acute phosphate nephropathy. For these patients, the guidelines recommend an alternative bowel preparation agent, polyethylene glycol, which is not associated with volume shifts and electrolyte abnormalities. Because patients must drink a large volume of this alternative bowel preparation agent, adherence can be an issue. In deciding whether to use a bowel preparation agent and in selecting which one to use, clinicians should carefully weigh the benefits and risks for each individual patient.8.Patients With Severe CKD Should Avoid Magnesium- or Aluminum-Containing Oral Preparations. Concomitant Use of Citrate-Containing Preparations and Aluminum-Containing Oral Preparations Is Potentially Hazardous Because It Can Lead to Acute Aluminum Toxicity.In patients with severe CKD, over-the-counter antacids that contain aluminum and magnesium (eg, Maalox and Mylanta) should be avoided. Other medications, such as the cathartic agent magnesium citrate, should likewise be used with caution. Indiscriminate use of magnesium-containing preparations can lead to severe hypermagnesemia. In addition, decreased renal function also increases the risk of aluminum accumulation and subsequent bone disease and neurotoxicity.28Alfrey AC Aluminum toxicity in patients with chronic renal failure.Ther Drug Monit. 1993; 15: 593-597Crossref PubMed Scopus (68) Google Scholar, 29Drüeke TB Intestinal absorption of aluminium in renal failure.Nephrol Dial Transplant. 2002; 17: 13-16Crossref PubMed Scopus (65) Google Scholar Chronic aluminum toxicity has been linked to sporadic Alzheimer disease and other neurodegenerative disorders30Yokel RA The toxicology of aluminum in the brain: a review.Neurotoxicology. 2000; 21: 813-828PubMed Google Scholar; however, this link is highly controversial. Moreover, certain medications, such as calcium citrate, potassium citrate, and sodium citrate, markedly enhance aluminum absorption from the gut. A number of studies have suggested that the concomitant use of citrate-containing preparations and aluminum hydroxide is potentially hazardous.31Coburn JW Mischel MG Goodman WG Salusky IB Calcium citrate markedly enhances aluminum absorption from aluminum hydroxide.Am J Kidney Dis. 1991; 17: 708-711Abstract Full Text PDF PubMed Scopus (62) Google Scholar, 32Walker JA Sherman RA Cody RP The effect of oral bases on enteral aluminum absorption.Arch Intern Med. 1990; 150: 2037-2039Crossref PubMed Google Scholar, 33Bakir AA Hryhorczuk DO Ahmed S et al.Hyperaluminemia in renal failure: the influence of age and citrate intake.Clin Nephrol. 1989; 31: 40-44PubMed Google Scholar In one such study, Kirschbaum and Schoolwerth34Kirschbaum BB Schoolwerth AC Acute aluminum toxicity associated with oral citrate and aluminum-containing antacids.Am J Med Sci. 1989; 297: 9-11Crossref PubMed Scopus (63) Google Scholar reported the development of a rapidly progressive encephalopathy marked by confusion, myoclonus, seizures, coma, and death in a group of women with renal failure who received an oral solution of citrate and aluminum hydroxide gel concurrently. Given these findings, patients with CKD who need to take a medication such as sodium citrate to prevent kidney stones or another citrate-containing preparation should not take aluminum hydroxide-containing medications. Because of the universal availability of such over-the-counter antacids, these patients should be advised of this specific contraindication.9.Although Most Patients With Hypertension Should Not Be Screened for Secondary Hypertension, Certain Clinical Clues May Suggest the Presence of an Underlying Cause That, When Addressed, May Resolve or Improve the Patient's Hypertension.From an epidemiologic standpoint, secondary hypertension is relatively uncommon. Of patients who are diagnosed as having hypertension in a primary care clinic, 95% have primary or essential hypertension, and only 5% have a secondary cause.35Danielson M Dammström B The prevalence of secondary and curable hypertension.Acta Med Scand. 1981; 209: 451-455PubMed Google Scholar In a study at a hypertension clinic, secondary hypertension accounted for only 9% of all patients seen.36Omura M Saito J Yamaguchi K Kakuta Y Nishikawa T Prospective study on the prevalence of secondary hypertension among hypertensive patients visiting a general outpatient clinic in Japan.Hypertens Res. 2004; 27: 193-202Crossref PubMed Scopus (409) Google Scholar Severe or difficult-to-control hypertension, hypertension that suddenly develops or suddenly worsens, or hypertension that is associated with other clinical findings may indicate secondary hypertension.37Trewet CL Ernst ME Resistant hypertension: identifying causes and optimizing treatment regimens.South Med J. 2008; 101: 166-173Crossref PubMed Google Scholar, 38Calhoun DA Resistant or difficult-to-treat hypertension.J Clin Hypertens (Greenwich). 2006; 8: 181-186Crossref PubMed Scopus (26) Google Scholar Hypokalemia may suggest primary aldosteronism; however, in 1 series, hypokalemia was present in only 25% of patients diagnosed as having primary hyperaldosteronism.36Omura M Saito J Yamaguchi K Kakuta Y Nishikawa T Prospective study on the prevalence of secondary hypertension among hypertensive patients visiting a general outpatient clinic in Japan.Hypertens Res. 2004; 27: 193-202Crossref PubMed Scopus (409) Google Scholar Headaches, palpitations, and sweats may suggest pheochromocytoma. Moon facies and/or striae may suggest Cushing syndrome, and a history of snoring in an obese patient may suggest obstructive sleep apnea. A bruit on one side of the abdomen may indicate renal artery stenosis. Worsening blood pressure or renal function on initiation of an ACEI or ARB may also suggest renal artery stenosis. Patients with peripheral vascular, cardiovascular, or cerebrovascular disease are at risk of also having renovascular disease. Other potentially correctable systemic conditions that can cause hypertension include hypothyroidism and hyperparathyroidism.Each of these findings or the already described historical features may suggest a secondary cause of the hypertension. Treatment of the underlying disorder can improve the patient's blood pressure and, in some instances, may resolve the patient's hypertension. Clinicians should determine whether the patient's medications (eg, NSAIDs, birth control pills, or certain decongestants) or lack of adherence to dietary restrictions (eg, ingestion of sodium and sodium-containing foods) is contributing to his or her suboptimal control and should review the patient's antihypertensive regimen for appropriateness. Assessment for target organ damage is also appropriate to determine cardiovascular risk. Determining when to evaluate for a secondary cause of hypertension is based on the pretest probability or the likelihood that 1 or more of the above historical features or physical findings are present. A stepwise approach should be used.10.In Patients With Recurrent Stone Disease, an Indepth Metabolic Evaluation Is Needed to Identify and Treat Modifiable Risk Factors, Thereby Preventing Further Episodes and/or Promoting Stone Dissolution.Nephrolithiasis, a common problem encountered by primary care physicians, can cause substantial morbidity. The likelihood that stone disease will develop in a man by age 70 years is as high as 1 in 8.39Fang LS-T Approach to the patient with nephrolithiasis.in: Goroll AH May LA Mulley AG Primary Care Medicine: Office Evaluation and Management of the Adult Patient. 4th ed. Lippincott Williams & Wilkins, Philadelphia, PA2000: 782-787Google Scholar The 10-year recurrence rates after a first calcium oxalate stone can be as high as 50% without treatment. It can be much higher in patients with a metabolic risk. As such, patients with an initial stone should undergo risk assessment. Patients with a family history of stones, concomitant gastrointestinal disease such as inflammatory bowel disease, frequent urinary tract infections, or a history of nephrocalcinosis should be referred to a nephrologist for further evaluation. Patients without these risk factors should have a simplified evaluation that includes a dietary history, a review of medications that can promote stone development, urinalysis, and measurement of levels of serum calcium, phosphorous, electrolytes, and uric acid.40Preminger GM The metabolic evaluation of patients with recurrent nephrolithiasis: a review of comprehensive and simplified approaches.J Urol. 1989; 141: 760-763PubMed Google Scholar Compositional stone analysis is an integral part of the metabolic evaluation because it can provide guidance for therapy.41Kourambas J Aslan P Teh CL Mathias BJ Preminger GM Role of stone analysis in metabolic evaluation and medical treatment of nephrolithiasis.J Endourol. 2001; 15: 181-186Crossref PubMed Scopus (53) Google Scholar The first-time diagnosis of a single calcium-containing kidney stone in a patient without a family history of kidney stones and with normal findings on an initial metabolic evaluation can be managed by increasing fluid intake to maintain a urine output of about 2 L/d. If a uric acid or cystine stone is detected on stone analysis, further metabolic evaluation with a 24-hour urine stone risk profile (eg, UroRisk or StoneRisk Panel [Mission Pharmacal Company, San Antonio, TX]) is warranted to guide both dietary and medical interventions.42Pak CYC Griggith DP Menin M Preminger GM Resnick MI ABCs of Medical Management of Stones. 2003 revised ed..http://www.abcsofstonedisease.com/Google Scholar Likewise, in patients without a stone available for analysis or in patients with multiple calcium stones, further metabolic evaluation, including the 24-hour urine stone risk profile, is recommended. Every new medication (prescribed, over-the-counter, and herbal) that is given to a patient with a renal allograft should be reviewed to determine if it will interact with his or her transplant medications (eg, tacrolimus or cyclosporine). Some medications may decrease calcineurin inhibitor levels; others may cause cyclosporine or tacrolimus toxicity.43Magee CC Pharmacology and side effects of cyclosporine and tacrolimus UpToDate Online 16.3.http://uptodateonline.com/online/content/topic.do?topicKey=tx_rheum/8690&selectedTitle=4∼150&source=search_resultsGoogle Scholar In both instances, the health of the patient or the success of the renal allograft may be jeopardized. For example, St Johns Wort, a herbal preparation, may decrease cyclosporine levels substantially, potentially resulting in acute rejection. Several other commonly prescribed medications that can be associated with reduced cyclosporine levels include rifampin, phenytoin, and carbamazepine. In contrast, diltiazem, verapamil, and erythromycin may increase cyclosporine levels. Cyclosporine can interfere with the metabolism of certain statins such as simvastatin, increasing the risk of statin-induced rhabdomyolysis. If any medication must be given to a patient with a renal allograft who is taking tacrolimus or cyclosporine, a careful review of its interaction with these medications should be made. If a drug must be used that has a considerable interaction, dose adjustment may be needed with careful follow-up of the calcineurin inhibitor levels. Careful monitoring is the rule. Renal disease is commonly encountered by primary care physicians. Early recognition, evaluation, and appropriate treatment and/or referral are necessary to moderate the substantial morbidity and mortality that are often associated with diseases of the kidney." @default.
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• W2017773190 title "The Top 10 Things Nephrologists Wish Every Primary Care Physician Knew" @default.
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