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Course # 34533 • Proteinuria and Hematuria

CASE STUDY 1

Patient G is a woman, 54 years of age, who was diagnosed with type 2 diabetes 20 years previously. She is currently taking metformin 1 gram twice every day and glyburide 5 mg twice daily. She is also prescribed amlodipine 10 mg/day for control of hypertension. At her yearly physical, Patient G is found to have a blood pressure of 154/86 mm Hg and a body mass index of 31. Her laboratory tests reveal a glycosylated hemoglobin (HbA1c) level of 9.4%, blood urea nitrogen (BUN) of 38 mg/dL, and a serum creatinine of 1.2 mg/dL. A routine urine dipstick performed in the office is negative. A urine test for microalbumin is sent to the laboratory, and the results show urine albumin of 125 mg/day, indicating microalbuminuria.

Comments and rationale : Proteinuria is one of the first signs of renal disease in patients with diabetes, and all type 2 diabetics should be screened yearly for microalbuminuria. It is unclear when Patient G was last screened, but she may be at risk for diabetic nephropathy.

Patient G is started on lisinopril 5 mg per day. She is asked to return in two weeks for a blood pressure check and to get repeat laboratory studies drawn.

At her return appointment, Patient G's blood pressure is 143/78 mm Hg, and her blood workup reveals a potassium level of 4.6 mEq/L and a serum creatinine level of 1.3 mg/dL.

Comments and rationale : ACE inhibitors, such as lisinopril, can cause a mild elevation in serum creatinine, likely due to decreased glomerular filtration, but this is not indicative of damage. Although it may appear that the patient's disease is worsening, ACE inhibitors are renal protective, as they appear to decrease the hyperfiltration that causes continuing renal injury. However, clinicians should always be aware of the need to modify prescribing based on a patient's renal function. Metformin is contraindicated in patients with elevated serum creatinine. Generally, women with a serum creatinine greater than 1.3 mg/dL and men with a serum creatinine greater than 1.4 mg/dL should not be prescribed metformin due to the increased risk of lactic acidosis.

Patient G is eventually titrated up to a dose of 40 mg of lisinopril. Although her blood pressure is now within the goal range at 124/73 mm Hg and her proteinuria has decreased to 40 mg/day, she has developed a persistent, dry cough that is worse at night.

Comments and rationale : The development of a persistent, non-productive cough is a common occurrence in patients taking ACE inhibitors. Although the exact rate is unknown due to likely under-reporting, up to 20% of all patients taking ACE inhibitors develop a cough. The only known curative treatment for ACE inhibitor-associated cough is stopping the medication, and resolution of the cough may take several weeks after the discontinuation of the medication. However, there are several medications that have been reported to be of benefit for cough suppression in patients for whom halting use of the ACE inhibitor is prohibited, including sodium cromoglycate, theophylline, sulindac, indomethacin, amlodipine, nifedipine, ferrous sulfate, and picotamide.

Patient G and her primary care provider discuss the benefits of ACE inhibitor therapy versus the discomfort of her current cough. Both are quite pleased with the decrease in the patient's proteinuria. The primary care provider discusses possibly switching to an ARB, which has shown benefit in decreasing proteinuria but does not induce cough. After carefully discussing the options and researching the subject, Patient G decides to stay on the ACE inhibitor. She has several relatives on dialysis and is motivated to avoid the consequences of chronic kidney disease. She tells her clinician that her research has revealed that ACE inhibitors have the strongest evidence for the prevention of the progression of renal disease in diabetic patients with proteinuria.

Comments and rationale : Clinicians should welcome an educated and motivated patient but also be aware that patients may obtain questionable or biased information in their own searches. It is important that clinicians have an understanding of available Internet resources and suggest reputable sites that can serve as a basis from which patients can begin their searches ( Resources ).

Patient W is a man, 59 years of age, with a history of smoking one pack per day for 40 years. He presents to his primary care provider with a 24-hour history of gross hematuria. Urinalysis reveals 30 RBCs per HPF. He denies burning on urination, flank pain, frequency, or fever. Patient W's primary care provider orders a CT of the pelvis with and without contrast and sends urine for cytology. She also arranges for urologic consultation.

Comments and rationale : Although hematuria is generally a benign finding, Patient W has several factors that are predictive of increased risk of malignancy, including older age, male gender, and greater hematuria (more than 25 RBCs per HPF). Gross hematuria is generally a urologic problem. While hematuria in men younger than 40 years of age is generally a benign finding, gross hematuria in men older than 50 years of age is a result of neoplasm in up to 25% of cases.

Although the CT scan and urine cytology are both negative, Patient W's urologist recommends a cystoscopy, due to his history of smoking and age. Cystoscopy shows a small superficial growth on the bladder wall, and pathology is positive for transitional cell cancer.

Comments and rationale : Smoking is associated with one-half of all bladder cancers. While there are identifiable risk factors for bladder cancer, such as smoking, there are currently no recommendations for routine screening of at-risk individuals.

Patient W's urologist reviews the cystoscopy findings and pathology report with him, as well as his previous CT report. Based on the results of these tests, the patient is diagnosed with transitional cell cancer of the bladder wall that does not involve the bladder muscle, classified as non-muscle-invasive disease. His urologist further informs him that while his disease has a potentially far better outcome than muscle-invasive disease, his staging is still based on the pathology of the tumor as well as the presence or absence of positive regional lymph nodes and the presence or absence of distant metastatic disease. He is told that his tumor is a T1 tumor that has invaded the subepithelial connective tissue. Because there are no positive regional lymph nodes or distant metastatic disease, his complete staging is T1N0M0. Patient W is scheduled for transurethral resection of the bladder tumor (TURBT).

Comments and rationale : Outcomes for bladder cancer patients vary widely depending on disease progression at time of presentation. Disease can be as low grade as noninvasive papillary carcinoma or as high grade as tumors that have invaded the pelvic and abdominal wall and have distant metastatic disease.

TURBT is the first step in the management of non-muscle-invasive bladder cancer. A TURBT is accomplished via cystoscopy, and it allows for both visualization and removal of suspicious tissue, thereby aiding both diagnosis and treatment. Tumors are completely resected, and other than for superficial appearing low-grade tumors, muscularis propria must be included in the removed tissue to ensure resection of all cancerous tissue. Management might include directed bladder biopsies of abnormal appearing urothelium or biopsies of the prostatic urethra to exclude difficult to visualize cancer. Biopsy or resection of the prostatic urethra also should be considered if the patient has tumor of the bladder neck or if the tumor is within the prostatic urethra.

CASE STUDY 2

Patient K is a man, 52 years of age, who works as a computer programmer. He presents to his primary care practitioner for an initial visit due to lower extremity edema. He denies chest pain, shortness of breath, polydipsia, or polyuria. He states that he is a smoker, having smoked one pack per day for the past 35 years. Patient K's family history is significant for his father dying from myocardial infarction at 64 years of age. He has no siblings. He does admit to occasional binge drinking and previous cocaine use.

On physical exam, Patient K appears tired. His vital signs are: blood pressure 153/67 mm Hg; pulse 84 beats per minute; respirations 18 breaths per minute; temperature 98˚F; weight 223 pounds; and height 6 feet. Physical examination reveals 2+ edema of the lower extremities and slight crackles at the bases of the lungs. Initial laboratory studies reveal a low serum albumin of 2.8 g/dL and an elevated cholesterol of 420 mg/dL. His triglycerides are 1400 mg/dL, and his fasting glucose is 103 mg/dL. His BUN is 28 mg/dL, and serum creatinine is 1.4 mg/dL. A urine dipstick test is performed in the office. It indicates 2+ protein, but no blood or glucose. A chest x-ray reveals slight bilateral infiltrates.

Comments and rationale : Patients with nephrotic syndrome often present with edema as their initial symptom. Although diabetes is the leading cause of nephrotic syndrome, other potential causes include infection (e.g., HIV, hepatitis), autoimmune syndrome, drug toxicity, and primary kidney disease.

Further laboratory studies reveal that Patient K is positive for hepatitis C, with a viral load of 3 million copies/mL. He is negative for HIV. The patient's HbA1c is 5.9%, and a 24-hour urine is positive for 3.7 grams of protein and a glomerular filtration rate of 57 mL/min/1.73 m2. He is referred to a nephrologist who confirms the diagnosis of nephrotic syndrome secondary to hepatitis C. The nephrologist starts the patient on an ACE inhibitor in an attempt to reduce the proteinuria, a low-dose diuretic to decrease edema, and atorvastatin to reduce the serum cholesterol level. Patient K is further referred to a liver specialist for treatment of his hepatitis C and to a dietician for diet counseling.

Comments and rationale : Treatment of nephrotic syndrome should address the primary cause of the syndrome as well as any associated lipid disorders, proteinuria, and edema. Dietary consultation may be necessary for many reasons, including low serum albumin, hyperlipidemia, weight management, and counseling regarding salt intake.

Six months later, Patient K has started interferon and ribavirin treatment for hepatitis C and his viral load is now undetectable. His proteinuria and hyperlipidemia have decreased significantly, and he has made significant lifestyle changes, including being tobacco-free for the last two months.

Comments and rationale : Lifestyle changes, such as diet, exercise, and eliminating use of drugs (including nicotine) and alcohol, are important in managing nephrotic syndrome. Nurses and dieticians are essential in helping to educate and motivate patients. Frequent visits may be needed, and clinicians should be careful not to overwhelm patients with a large amount of information at one time. Clinicians should also use easily understood printed materials that patients can take home and refer to frequently.

Patient S is a woman, 35 years of age, who was diagnosed with lupus 12 years previously. She has had a reasonably mild course, having been treated with hydroxychloroquine and low-dose ibuprofen as needed for joint pain. She presents to her primary care practitioner with fatigue and peripheral edema. Laboratory analysis reveals a BUN of 68 mg/dL, serum creatinine of 2.8 mg/dL, hematocrit of 28%, and serum albumin of 2.3 g/dL. A urine dipstick performed in the office is positive for blood and 1+ protein. A tentative diagnosis of lupus nephritis is made, and Patient S is urgently referred to her rheumatologist.

Comments and rationale : Early detection of lupus nephritis is essential to reduce morbidity and mortality. The goals of treatment should include reduction in proteinuria and slowing of the disease progression. Corticosteroids in combination with immunosuppressants (cyclophosphamide, azathioprine, and mycophenolate mofetil) are the mainstay of treatment. Use of immunosuppressants is associated with reduced mortality and improved renal outcomes. Clinicians should be aware of the side effects of prescribed medications and should educate patients both of possible side effects and management techniques. While patients may initially resist referral to a mental health provider, the provision of mental health services can be very beneficial, both in helping to manage the psychiatric side effects of treatment and to support the patient in the long term. Many patients with systemic lupus erythematosus experience stress and severe depression. Corticosteroids can cause multiple side effects ranging from insomnia, weight gain (with resultant change in body image), hypomania, psychosis, depression, and irritability.

Few diseases call for as much clinician support and education as systemic lupus erythematosus. Patients with lupus nephritis may feel overwhelmed and hopeless, but a caring clinician can help empower patients by educating them regarding disease management, proper diet and medication adherence, and a healthy lifestyle.

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