Morning o g Report: epo 60 y.o. man with pink urine 10/27/10 Edward Ed dG Gometz t Shana Ratner Diane Altkorn MKSAP • • A 52-year-old man is evaluated for a 3-month history of perineal and suprapubic pain. He has experienced urinary frequency and dysuria for 4 to 6 weeks. The patient reports fatigue, insomnia, and low mood for the past 6 months. He has hypertension. Current medications are hydrochlorothiazide and acetaminophen as needed for pain. On physical examination, temperature is normal, blood pressure is 138/80 mm Hg, and pulse rate is 78/min. BMI is 29. Abdominal examination is normal with mild suprapubic tenderness. The prostate is not enlarged; it is mildly tender without nodularity. Testicular examination is normal. MKSAP • On laboratory study, urinalysis is normal, and urine culture is negative. Prostate-specific antigen level is 0 8 ng/mL (0 0.8 (0.8 8 µg/L) µg/L). • Which of the following is the most appropriate p treatment for this patient? • A Levofloxacin • B Naproxen • C Oxybutynin • D Saw palmetto • E Terazosin T i MKSAP • On laboratory study, urinalysis is normal, and urine culture is negative. Prostate-specific antigen level is 0 8 ng/mL (0 0.8 (0.8 8 µg/L) µg/L). • Which of the following is the most appropriate p treatment for this patient? • A Levofloxacin • B Naproxen • C Oxybutynin • D Saw palmetto • E Terazosin T i MKSAP Answer • • • Chronic prostatis/chronic pelvic pain syndrome manifestations: – GU/pelvic pain – Voiding g symptoms y p – Urine culture negative – Presence or absence of leukocytes in the urine has little clinical utility – There are no lab or diagnostic findings Among pharmacologic therapies, efficacy data is strongest for use of alpha blockers in treating chronic prostatitis and chronic pelvic pain syndrome d There is no evidence for a bacterial cause. – It is common practice to prescribe 4-6 weeks of antibiotics, but there is lack of clinical trial evidence The Case 60 y/o man hx CKD, HTN p/w 2 day hx of urine that looks like “pink p lemonade” HPI • Urinaryy – Mild dysuria (stinging pain) started today – Increased frequency and urgency for past week – Right sided lower back and flank pain intermittent for past 5 days – Noticed urine was reddish for p past 2 days y • ROS – 30lb weight loss over 12 months (unintentional) – No recent fevers, but occasional night sweats/chills for weeks – Occasional postprandial abd pain and nausea. Denies vomiting, diarrhea History Past Medical History • • • • • Chronic Kidney Disease, stage IV Hypertension Uveitis Spinal Surgery (1995) • Family Hx • • • • • • • Both parents deceased, deceased had hypertension Social Hx w w Allergies Married, retired, 3 children 40 pyh tob, significant alcohol abuse (quit 1 year ago), no IVDU NKDA Home Medications • Amlodipine/ Benazepril 5mg5mg 20mg daily Carvedilol 25 mg BID Minoxidil 2.5mg gq qAM Minoxidil 5 mg qPM Thiamine 100mg daily Folate 1mg g daily y Colace 100 mg daily Tums 1 to 2 tabs with meals Physical Exam y Vitals: T 361 P 82 BP 130/69 R 18 O2 Sat 96% RA y Gen: A&OX3, in NAD y HEENT: PERRLA, EOMI, poor dentition, clear oral pharynx, no , ,p , p y , y y y y y y y pallor, no scleral icterus, mildly injected sclera Neck: No lymphadenopathy, no neck mases CVS: RRR, nl S1 & S2, no m/r/g, no JVD Extremities: Warm, pulses 2+ bilaterally, no edema Lungs: Non‐labored respirations, CTA bilaterally Abd: Soft, hypoactive bowel sounds, non‐distended, slight right yp g g flank tenderness, palpable liver below costal angle Neuro: CN intact, UE & LE strength 5/5, sensation intact Skin: no rashes or lesions Initial Labs (10.5‐12.0) 11.7 134 109 35 208 7.6 33.3 MCV 82.2 N 56 L 30 M 14 E 2 12.3 1.7 124 3.5 15 2.7 3.2 (2.3‐2.7) AG 10 7.4 Urinalysis: leuk est +, nitrite -, Prot 3+, Bl d 3+ Blood Ionized Ca++: 7.26 (NR:4.6-5.4) Lipase: 60 3.5 03 0.3 31 26 84 Initial Labs (10.5‐12.0) 11.7 134 109 35 208 7.6 33.3 MCV 82.2 N 56 L 30 M 14 E 2 12.3 1.7 124 3.5 15 2.7 3.2 (2.3‐2.7) AG 10 7.4 Urinalysis: leuk est +, nitrite -, Prot 3+, Bl d 3+ Blood Ionized Ca++: 7.26 (NR:4.6-5.4) Lipase: 60 3.5 03 0.3 31 26 84 Differential • Initial differential • Initial management • What next? Urine microscopy Imaging? • Renal Ultrasound: Renal calculus. Hydroureter and hydronephrosis. • CT Abd/ Pelvis: Right ureteral stent in anatomic position, resolving hydronephrosis, evidence of hydroureter with renal calculus present on right side. Moderately enlarged prostate without bladder distension. No other abnormalities noted. Types of kidney stones Types of Kidney Stones • Calcium ((Oxalate or Phophate) p ) – Most common type of kidney stone (80-85%) – Can occur in hyper and hypo calcemia – Inability I bilit tto process oxalate l t rich i h ffoods d effectively ff ti l • Struvite – Less common type yp of kidney y stone ((10-15%)) – Infectious (most commonly Proteus mirabilis, also Klebsiella • Uric acid – Much less common type of kidney stone (~5-10%) – Seen with conditions that promote hyperuricosuria (low pH) • Cystine – Rare type of kidney stone (most often linked to genetic defect) Clinic management of kidney stones Confirm Diagnosis • KUB can help assess stone burden, size, and location; • Intravenous Urography (gold standard) • Renal U/S can also be adequate to assess a stone but also look for hydronephrosis/ hydroureter • CT is rarely used for stone assessment alone and usually locates a stone as an incidental finding Assess severity • Stone size, location, and patient symptoms all are implicated in determining whether you have an urological emergency vs. conservative management. Clinic management of kidney stones Medical Expulsive Therapy •Analgesia •Stone retrieval strategies •Extracorporeal shock wave lithotrypsy •“Ureteral-relaxing” g medications - Nifedipine - Tamsulosin - Prednisone Back to the case • Patient with nephrolithiasis 134 109 12.3 35 124 3.5 15 2.7 1.7 3.2 Spectrum of Hypercalcemia Spectrum of hypercalcemia indicated by serum total and ionized calcium levels. Differential for Hypercalcemia?? Hypercalcemia Manifestations Renal “stones” Nephrolithiasis Nephrogenic diabetes insipidus Dehydration Nephrocalcinosis Skeleton “bones” Bone pain Arthritis Osteoporosis Osteitis fibrosa cystica in hyperparathyroidism (subperiosteal resorption, bone cysts) Gastrointestinal “abdominal moans” Nausea,, vomiting g Anorexia, weight loss Constipation Abdominal pain Pancreatitis Peptic p ulcer disease Neuromuscular “psychic groans” Impaired concentration and memory Confusion, stupor, coma Lethargy and fatigue M Muscle l weakness k Corneal calcification (band keratopathy) Cardiovascular Hypertension Shortened QT interval on electrocardiogram g Cardiac arrhythmias Vascular calcification Other Itching Keratitis, conjunctivitis Differential for Hypercalcemia Parathyroid hormone-related Medications Primary hyperparathyroidism* Sporadic familial Sporadic, familial, associated with multiple endocrine neoplasia I or II Tertiary hyperparathyroidism Associated with chronic renal failure or vitamin D deficiency y Thiazide diuretics (usually mild)* Lithium Milk-alkali syndrome (from calcium antacids) Vitamin A intoxication (including analogs used to treat acne) Other endocrine disorders Vitamin D-related Vitamin D intoxication Usually 25-hydroxyvitamin D2 in over-the-counter supplements l t Granulomatous disease sarcoidosis, berylliosis, tuberculosis Hodgkin's lymphoma Hyperthyroidism Adrenal insufficiency Acromegaly Pheochromocytoma Genetic disorders Familial hypocalciuric hypercalcemia: mutated calcium-sensing receptor Malignancy Other Humoral hypercalcemia of malignancy* (mediated by PTHrP) Solid tumors, especially lung, head, and neck squamous cancers, renal cell tumors Local osteolysis* (mediated by cytokines) multiple myeloma, breast cancer Immobilization, with high bone turnover (e.g., Paget's disease, bedridden child) Recovery phase of rhabdomyolysis Work Up? • PTH: 7 (NR: 15-75) Work-Up • CT Abd/ Pelvis: as reported before, no evidence of malignancy li • Chest X-Ray: X Ray: Prominent hilar lynphadenopathy, large pulmonary arteries, bibasilar scarring, no acute abnormalities • • • • • • PTHrH: Negative Alk Phos: 84 (NR: 30-120) Protein Electrophoresis: Negative for Myeloma Calcitriol (1,25 Dihydroxy Vit D): Elevated TSH 2.6 TSH: 2 6 (NR (NR: 0 0.3-4.0) 3 4 0) PSA: 1.6 CT Chest Granuloma vs. Lymphoma • • • • Clinical and serological evidence for both diagnosis. ACE level: <5 (NR: 8-52) – ACE level known to be unhelpful in diagnosing sarcoid when patient ti t is i taking t ki an ACE-I ACE I (our ( ptt taking t ki Benazepril) B il) c-ANCA: Negative (eval for Wegener's granulomatosis) PPD: Negative What next? • Consult pulmonology for bronchoscopy Bronch results Sarcoidosis - Epidemiology • Affects both genders, but more prominent in women. • The lifetime risk of sarcoidosis for U U.S. S whites is estimated at 0.85 percent compared with 2.4 percent in U.S. blacks. Sarcoidosis is most prevalent in S d Swedes, D Danes, and dU U.S. S bl blacks. k • The condition usuallyy p presents in adults yyounger g than 40 years, most frequently between 20 and 29 years of age. Sometimes incidentally found in older people g y asymptomatic. y p if theyy are largely Sarcoidosis - Causes • Causes include genetic inheritance, infectious transmission, and shared exposure to environmental agents agents. • Infectious organisms such as viruses, mycobacteria, Borrelia burgdorferi and Propionibacterium acnes have been implicated burgdorferi, as potential causes of sarcoidosis. • Environmental exposure to beryllium beryllium, aluminum aluminum, and zirconium can result in a granulomatous response similar to that of sarcoidosis. • Current theory suggests that disease develops in genetically predetermined hosts who are exposed to certain environmental agents that trigger an exaggerated inflammatory immune response leading to granuloma formation formation. Sarcoidosis - Organs Sarcoid - Therpies • Systemic Corticosteroids • Inhaled Corticosteroids • Cytotoxic C t t i Agents A t (methotrexate ( th t t and d azathioprine) thi i ) • Immunomodulators • Surgical g Intervention Hospital course •Urology Urology consulted and placed stents for severe hydronephrosis •IV fluids were immediately started to bring down the Ca++ •Creatinine remained stable •Stone Stone passed and found to be composed of calcium oxalate •After 1 day, hematuria had started to clear, and flank pain had resolved. Urine culture taken and patient was treated empirically with Ciprofloxacin. Ciprofloxacin •Patient’s calcium level was 10.4 (~6.3 ionized) on discharge home. •Patient was scheduled to follow up with pulmonology clinic as an outpatient. Take home points • Makeup of kidney stones • Outpatient management of kidney stones • Initial management and differential for hypercalcemia • Overview O i off sarcoidosis id i References • Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1;67(9):1959-66. ; ( ) • Wu JJ, Schiff KR. Sarcoidosis. Am Fam Physician. 2004 Jul 15;70(2):312-22. • http://www.kidneyatlas.org/book4/adk4-08.pdf http://www kidneyatlas org/book4/adk4 08 pdf • www.herringlab.com • Up p To Date • Merck Manual Online • Wikipedia