Renal Board Review – Part I

Renal Board Review – Part I
April 4, 2013

53yo man has a 3 week history of increasing weakness and anorexia
53yo man has a 3 week history of increasing weakness and anorexia. He takes no medications. On exam BP 130/70, HR 80 without orthostatic changes. No JVD, rales, or LE edema. Labs: BUN 12, Creat 0.8, Na 123, K 3.4, Cl 91, Bicarb 22, Serum Osm 270, Urine Osm What is the most likely cause of this patient’s hyponatremia? Mineralocorticoid deficiency Low solute diet Nephrotic syndrome SIADH

A 44-year-old man is evaluated in the hospital because of disorientation and hallucinations. He was admitted to the hospital 4 days ago for a subarachnoid hemorrhage that was repaired with surgical clipping. His medical history is otherwise unremarkable. On physical examination, he is disoriented, confused, and hallucinating. Temperature is normal, blood pressure is 140/80 mm Hg, pulse rate is 90/min, and respiration rate is 16/min. Upon standing, his blood pressure is 120/60 mm Hg and pulse rate is 110/min. The remainder of the physical examination is normal. Laboratory values were normal on admission, but now reveal: Na 118, K 4.1, Cl 85, Bicarb 23, Serum Osm 248, Uric acid 6.8, Spot urine Na 105, Urine Osm 633 Which of the following is the most likely cause of his hyponatremia? Glucocorticoid insufficiency Cerebral salt wasting Hypothyroidism Syndrome of inappropriate antidiuretic hormone secretion

A 22-year-old woman is evaluated at an on-site medical center after collapsing while running a marathon. She is disoriented. During the evaluation, she experiences a generalized tonic-clonic seizure lasting 3 minutes. A wristband indicates that she has DM1. On exam, BP 120/60, temp normal, HR 100, RR 28. She is confused but has no evidence of a focal neurologic deficit. Glc 120, Na Which of the following is the most appropriate next step in this patient’s management? 3% saline infusion 50% glucose by intravenous bolus Intravenous furosemide Normal saline infusion

Hyponatremia Goal: increase by 0.5/hr (no more than 10/24h)
Plasma Osmolality Low (<275) Check Volume Status Hypovolemic Renal Losses (Una >20) Diuretics Mineralocorticoid insufficiency Salt-wasting nephropathy Cerebral Salt Wasting Extrarenal Losses (Una <10) Vomiting/Diarrhea Insensible losses Third spacing (Pancreatitis) Euvolemic Appropriately Low Uosm (<100) Primary Polydypsia Low solute diet/Beer potomania Inappropriately high Uosm SIADH Hypothyroidism Glucocorticoid insufficiency Hypervolemic Nephrotic Sx CHF ESLD ESRD Normal PseudohypoNa Isosmotic irrigating solution High (>295) Mannitol Hyperglycemia Goal: increase by 0.5/hr (no more than 10/24h) If treat too quickly, will cause CPM (seizures, AMS, paresis, resp dysfunction, etc)

Hypernatremia 5.4L Etiologies: Treatment Defective thirst mechanism
Inadequate access to water (elderly in nursing home) Kidney concentrating defect (DI) – to be discussed further in Endo section **Loss of hypotonic fluids with inadequate water replacement (GI, kidney, skin) Treatment Correct slowly to avoid cerebral edema (Goal: 50% corrected in hours) First, make sure patient is volume replete (use isotonic saline) Then, replace free water Free water deficit = TBW x [(Plasma Na/140)-1] TBW = 0.6 x kg (male) or 0.5 x kg (female) Ex: 75kg female who appears euvolemic with Na of 160 TBW = 0.5(75) = 37.5 Free water deficit = 37.5 [(160/140)-1] = 5.4L

Adrenal insufficiency Impaired kidney potassium excretion
A 23-year-old man with HIV infection is evaluated in the hospital for the recent onset of hyperkalemia. He was admitted to the hospital 1 week ago for severe Pneumocystis jirovecii pneumonia; TMP-SMX and corticosteroids were begun at that time. For the past 2 months, he has been taking highly active antiretroviral therapy. Physical examination is unremarkable, and there is no evidence of hypovolemia or edema. Labs on Admission: Na 131, K 4.8, Cl 95, Bicarb 22, BUN 20, Creat 1.3 Labs Today: Na 132, K 6.2, Cl 104, Bicarb 18, BUN 21, Creat 1.4 Which of the following is the most likely cause of this patient’s hyperkalemia? Adrenal insufficiency Impaired kidney potassium excretion Lactic acidosis Proximal renal tubular acidosis Rhabdomyolysis Bactrim inhibits sodium reabsorption in the distal nephron, which leads to a decrease in luminal electronegativity and subsequent inhibition of potassium secretion. Prox RTA causes hyPOkalemia.

Hyperkalemia Etiologies/Mechanisms: EKG changes Treatment
Potassium shifts (from intracellular to extracellular): Rhabdo, hemolysis, hyperosmolar states, insulin deficiency, beta-blockers, metabolic acidosis Excessive intake (citrus, salt substitutes) - rare Decreased kidney excretion Acute/Chronic CKD; Low flow states (decreased filtration = decreased excretion) Hyporeninemic Hypoaldosteronism (decreased Aldo = decreased Na/K exchange) Seen in DM nephropathy Seen with certain meds (ACEI, Aldo antagonists, NSAIDS) Inhibition of distal tubule Na transport (inhibition of Na resorption = cannot secrete K) Druge: amiloride, triamterene, TMP-SMX Sickle Cell nephropathy; other interstitial diseases EKG changes Treatment

Hypokalemia Etiologies/Mechanisms:
Potassium shifts (from extracellular to intracellular) Inhaled beta-agonists, insulin, hypothermia, excess catecholamines, metabolic alkalosis Total body depletion (associated with low urine chloride) Vomiting, diarrhea Increased Kidney Excretion Hyperaldosteronism Diuretics Magnesium deficiency EKG changes: ST depression, T wave flattening/inversion, increased U wave Treatment

A 47-year-old man with a long-standing history of alcoholism is hospitalized for abdominal pain, nausea, and vomiting of 7 days’ duration. He has lost approximately 10% of his body weight over the past 4 months. On physical examination, he appears cachectic. HR 110, other vitals wnl. There is midepigastric tenderness without rebound. Bowel sounds are present. Neurologic examination is normal. The patient receives immediate thiamine replacement, folic acid supplementation, and a multivitamin followed by vigorous intravenous fluid replacement with 5% dextrose and normal saline with aggressive potassium replacement. Morphine is used to control pain. Eighteen hours later, the patient’s abdominal pain has improved but he becomes restless, agitated, and extremely weak and is barely able to raise his extremities against gravity. Which of the following is the most likely cause of this patient’s new findings? Hypercalcemia Hypokalemia Hyponatremia Hypophosphatemia

Hypophosphatemia Phos: Kidney secretes 90% but reabsorbs 80% via prox tubule
Etiologies/Mechanisms Cellular redistribution (extracellular to intracellular) Refeeding syndrome after starvation Insulin administration for severe hyperglycemia Hungry Bone syndrome after parathyroidectomy Respiratory alkalosis Decreased intestinal absorption Antacids Chronic diarrhea with malabsorption Inadequate Intake: alcoholics, starvation Increased Urinary Excretion Fanconi Syndrome (i.e. prox tubule dump syndrome) Osmotic diuresis (glycosuria) Secondary Hyperparathyroidism

Acid/Base Questions Method: Primary disorder?
Appropriate Compensation? Anion gap? Delta-delta? Osmolar gap? Delta-delta = Anion gap Bicarb Delta-delta >1 = also a metabolic alkalosis present Delta-delta <1 – also a NAGMA present

Distal (type 1) renal tubular acidosis Hypertensive nephrosclerosis
A 65-year-old man is evaluated for a 3-month history of progressive malaise, fatigue, and weakness. He has a 10-year history of hypertension treated with hydrochlorothiazide and atenolol. Labs are normal. Labs: WBC 5600, Hct 25%, Plt 340k, Glc 110, Na 135, K 3.0, Cl 107, Bicarb 18, BUN 22, Creat 1.8, UA pH 5.5 trace protein and 1+ glc urine protein/creat ratio: 4.8mg/mg ABG: 7.33/28/98 on RA Polarized light microscopy of urine sediment is normal Which of the following is the most likely diagnosis? Diabetic nephropathy Distal (type 1) renal tubular acidosis Hypertensive nephrosclerosis Proximal (type 2) renal tubular acidosis Multiple myeloma is one of many diseases that can cause the combination of RTA and proximal tubule dysfunction known as Fanconi syndrome. Multiple myeloma is consistent with this patient’s anemia; mildly elevated serum creatinine level; and significant proteinuria despite only trace protein detected on dipstick urinalysis, which suggests the excretion of a cationic protein compatible with the immunoglobulin secretion associated with multiple myeloma. RTA is characterized by a normal anion gap metabolic acidosis, hypokalemia, and an intact ability to lower the urine pH

Alcoholic ketoacidosis Ethylene glycol toxicity Methanol toxicity
A 19-year-old man is evaluated in the emergency department for altered mental status. He is accompanied by a friend, who states that the patient was asymptomatic 12 hours ago. No PMHx. He does not drink alcoholic beverages or use illicit drugs. On physical examination, the patient is comatose. Afebrile, sats 95% on RA, BP 90/60 mm Hg, HR 110/min, and RR 28/min. Cardiopulmonary examination is normal. There are no localized findings on neurologic examination. Labs: Glc 114, Na 142, K 3.6, Cl 108, Bicarb 14, BUN 14, Serum Osm 290, UA 1+ketones ABG: 7.42/20/94 on RA Which of the following is the most likely cause of this patient’s acid-base disorder? Alcoholic ketoacidosis Ethylene glycol toxicity Methanol toxicity Salicylate toxicity AG of 20!! Winter’s formula: Expected PCO2 = 1.5 × [Bicarbonate] + 8 ± 2 mm Hg, so in this patient, expected pCO2 with bicarb of 14 is pCO2 is too low, thus a respiratory alkalosis also present. Also, the other 3 would also give you an elevated osmolar gap, which this patient does not have (Osm gap = 5).

Alcoholic ketoacidosis Methanol poisoning Ethylene glycol poisoning
A 56-year old man with a history of alcoholism is found lying on the street. On arrival at the emergency department, he is confused. On physical examination, temperature is 36.1 °C (97.0 °F), blood pressure is 126/80 mm Hg, and pulse rate is 70/min. Funduscopic examination shows no papilledema. Cardiac, pulmonary, and abdominal examinations are normal Labs: Glc 86, BUN 45, Creat 2.8, Na 138, K 5.4, Cl 98, Bicarb 14, Serum Osm 316, UA with calcium oxalate crystals. ABG: 7.28/29/80 on RA Which of the following is the most likely diagnosis? Alcoholic ketoacidosis Methanol poisoning Ethylene glycol poisoning Lactic acidosis +Metabolic acidosis, AG = 16, Osm gap = 20; oxalate crystals in urine = ethylene glycol (which also causes renal failure). Methanol -> formic acid byproducts which affect eyes

Metabolic Acidosis AGMA – MUDPILES NAGMA – HARDUP RTAs
(Hyperalimentation, Acetazolamide, RTAs, Diarrhea, Ureteroenteric fistula, Pancreatic fistula) RTAs Type II (Proximal) Type I (Distal) Type IV

Type II RTA (proximal) Can have isolated RTA, but more often than not, it is due to generalized dysfunction of the tubule Proximal tubule usually responsible for reabsorbing a number of different solutes glc, phos, amino acids, uric acid, protein, potassium, and BICARB All these are now excreted instead of reabsorbed (Fanconi’s Syndrome) Bicarb is excreted -> NAGMA Bicarb usually around and VERY difficult to treat with supplemental bicarb PO bicarb rapidly excreted in urine and can’t be reabsorbed PO bicarb can actually worsen hypokalemia Causes: Multiple Myeloma SC disease Heavy Metals (wilson’s Lead, Mercury) Drugs (Ifosfamide) Acetazolamide Complications: Osteomalacia 2/2 chronic hypophos Osteoporosis 2/2 acidosis-induced demineralization of bone Treatment: Can add thiazide to decrease blood volume-> decrease GFR -> decrease bicarb filtration Can consider aldactone to help with potassium wasting

Type I RTA (distal) Problem with H-ATPase – cannot excrete H+ (via NH4+) thus cannot acidify urine -> NAGMA More severe acidosis!! Bicarb ~10 Severe hypokalemia ++UAG Urine is electroneutral Unmeasured anions neutralized by Na and K; unmeasured cations (typically NH4+) neutralized by Cl UAG = (UNa+UK) – UCl In Type I RTA, NH4+ cannot be excreted. Decreased unmeasured cations = decreased Ucl needed to neutralize them, so will give you a net ++ urine anion gap Causes: Autoimmune (Sjogren’s, SLE) Drugs (AmphoB, Lithium) Genetics Complications: Nephrolithiasis & nephrocalcinosis Due to severe acidosis and its effect on bone mineral dissolution Treatment: Correct K deficit prior to correcting acidosis PO alkali therapy (1-2meq/kg daily) to neutralize acid

Type IV RTA Not actually a disorder of the tubules
Due to aldosterone deficiency/resistance in the distal tubules & collecting ducts Affects Na/K ATPase -> hyperkalemia (decreased excretion) Elevated potassium impairs NH4+ excretion into urine, thus left with NAGMA (less so than seen with Type I RTA) Also have small +UAG Causes: Diabetes Mellitus Chronic Interstitial Nephritis Meds (Aldactone, ACEI, NSAIDs, Trimethoprim) Treatment: Correct underlying hyperkalemia (this should restore NH4+ excretion and fix acidosis) Can try PO alkali therapy Stop offending meds Increase distal sodium delivery to stimulate K and H secretion Fludrocortisone if not hypertensive Thiazide if HTN +/- loop diuretic (if GFR <30) If aldosterone resistance present, cannot take in Na in exchange for K, so you build up K

Alcoholic ketoacidosis Diabetic ketoacidosis Ethylene glycol
A 32-year-old man is brought to the emergency department after becoming disoriented, combative, and agitated earlier that day. He is accompanied by a friend, who states that the patient has a history of alcohol and drug abuse, including inhalants. On physical examination, the patient is uncooperative and slightly disoriented. Temperature is normal, blood pressure is 140/88 mm Hg, and pulse rate is 98/min. The remainder of the examination is normal. Glc 110, Na 142, K 4.1, Cl 109, Bicarb 23, BUN 18, Serum Osm 320, Creat 1.1, serum ketones +, UA with trace glc and 4+ ketones, ABG: 7.4/44/92 on RA Which of the following is the most likely cause of this patient’s clinical presentation? Alcoholic ketoacidosis Diabetic ketoacidosis Ethylene glycol Isopropyl alcohol Toluene Osmolar gap: Serum Osm – [2(Na) + Glc/18 + BUN/2.8] In this patient: 320-[2(142)+110/18+18/2.8] = = 23 No anion gap **Isopropyl alcohol Toluene = inhalant that causes similar symptoms, but metabolic acidosis and hypokalemia

Osmolar Gap Serum Osm – [2(Na) + Glc/18 + BUN/2.8] Causes: Alcohols
Ethylene Glycol Methanol Isopropyl Alcohol Acetone Sugars Mannitol Sorbitol Lipids Hypertriglyceridemia Proteins Hypergammaglobulinemia

Begin hydrochlorothiazide Begin sodium citrate
A 35-year-old man comes for a follow-up evaluation for recurrent symptomatic calcium oxalate kidney stones. His episodes of nephrolithiasis are associated with significant pain and are disabling. His last attack was 1 month ago. He first developed kidney stones 5 years ago and typically has one to two episodes each year. He has been adherent to recommendations to increase his fluid intake and maintain a low-sodium diet. On physical examination, vital signs are normal. BMI is 26. The remainder of the examination is unremarkable Workup: UA: pH 5.0 (normal ), 1+ blood, no protein, 0-3 RBCs/hpf, no bacteria, no glc Urine Ca excretion: 230mg/24h (nml mg/d) Urine citric acid excretion: 350mg/24h (nml mg/d) Urine oxalate excretion: 140mg/24h (nml mg/d) In addition to avoiding foods high in oxalate and adhering to a low-protein diet, which of the following is the most appropriate next step in this patient’s management? Hyperoxaluria!! (normal calcium and citrate urinary output) PO Ca binds oxalate in the gut and prevents its absorption, thus preventing excretion in urine and formation of stones Begin allopurinol Begin hydrochlorothiazide Begin sodium citrate Increase dietary calcium intake

A 56-year-old man comes for a follow-up examination
A 56-year-old man comes for a follow-up examination. Two weeks ago, he was evaluated in the emergency department for acute flank pain caused by a passed uric acid stone; since then, he has been asymptomatic and has felt well. He believes he had a kidney stone 5 years ago but did not seek medical attention at that time. He has hypertension and a 3-year history of infrequent gouty attacks. His only medication is lisinopril. On physical examination, temperature is normal, blood pressure is 132/80 mm Hg, pulse rate is 70/min, and respiration rate is 18/min. BMI is 21. The remainder of the examination is unremarkable. Urinalysis shows a urine pH of 5.5, but no blood/protein. In addition to increasing PO fluid intake, which of the following is the next best step in management of this patient? Allopurinol Hydrochlorothiazide Potassium citrate Probenecid Uric acid stones – treatment includes urine alkalination with potassium citrate. Most experts only use allopurinol to reduce urine uric acid excretion in patients with hyperuricosuria in whom alkalinization is difficult, poorly tolerated, or not completely effective. In addition, reducing urine uric acid excretion with allopurinol would be relatively ineffective in patients with a low pH. Furthermore, this patient has borderline hyperuricemia and infrequent gouty attacks and may not need prophylactic allopurinol, which is typically used in patients with one to two acute gouty attacks per year

Kidney Stones ~80% ~10% ~10% ~1-3%

Kidney Stones Calcium Oxalate Stones (~80%) Uric Acid Stones (10%)
3 mechanisms: Hypercalciuria (**most common) **Need to increase Ca intake (binds Oxalate in gut and prevents its absorption) thiazides Hyperoxaluria **need to increase Ca intake avoid high oxalate foods (rhubarb, peanuts, spinach, chocolate) Hypocitrauria (citrate normally binds Ca in urine and prevents it from binding oxalate Need to increase citrate (lemon juice or potassium citrate) Uric Acid Stones (10%) Seen in Gout, Tumor Lysis Syndrome Treatment: Urine alkalinization (potassium citrate) Allopurinol (after attempting to alkalinize urine) Struvite Stones (10%) Increased risk with recurrent Klebsiella or Proteus UTI Need to acidify urine!! (i.e. cranberry juice) If not treated, can lead to Staghorn Calculi If infected, need Abx and referral to urology Cysteine Stones (1-3%) Often due to genetic defect leading to increased cysteine excretion Tx: Alkalinization of urine

A 26-year-old man is evaluated in the emergency department for a 1-day history of acute abdominal pain that has progressively worsened. He has pain in the left flank that radiates to the groin. He also has nausea and vomiting. Ibuprofen has not provided relief. On physical examination, temperature is normal, blood pressure is 168/98 mm Hg, pulse rate is 100/min, and respiration rate is 18/min. BMI is 28. Abdominal examination reveals left costovertebral angle tenderness. Serum creatinine 1.5 Urinalysis: pH 5.0, 2+ blood, 1+ Leuk esterase, 2-5 WBC/hpf, RBC/hpf, no bacteria Noncontrasted CT of the abdomen reveals 4-mm calculus in the mid left ureter and mild hydronephrosis In addition to analgesic, which of the following is the most appropriate management for this patient? Extracorporeal shock-wave lithotripsy Intravenous cephalexin Intravenous saline Percutaneous nephrostomy

A 52-year-old woman is evaluated for dysuria, urinary frequency, and lower abdominal pain of 2 days’ duration. Medical history is significant for urinary tract infection that occurs three to four times yearly. She also has hypertension treated with amlodipine. On physical examination, temperature is 37.4 °C (99.3 °F), blood pressure is 152/96 mm Hg, pulse rate is 80/min, and respiration rate is 18/min. BMI is 41. The remainder of the examination is normal except for mild suprapubic tenderness Labs: WBC 7,000; BUN 12; Creatinine 1.0; Urinalysis pH 8.0, 1+ blood; 3-5 RBC/hpf; leukocyte clumps, + leuk esterase, + nitrites. Abdominal CT reveals a 4-cm staghorn calculus on R kidney. Which of the following is the most appropriate next step in this patient’s management? Extracorporeal shock-wave lithotripsy Intravenous cephalexin Percutaneous nephrolithotomy Start potassium citrate

Acute Management of Kidney Stones
Symptomatic Stone Size of stone <5mm >7mm 5-7mm Hydration Analgesia CCB/a-blocker/steroids Lithotripsy (ESWL) stones <1cm in kidney or prox urinary tract (bust up the stones) Ureterorenoscopy scope into distal ureter to remove stone (or parts of larger stone already broken up by ESWL) Perc nephrolithotomy For stones >1cm, any staghorn or cysteine Fail to pass Locate stone CCB dilate ureteral smooth muscle; a-blockers decrease ureteral spasm; steroids decrease inflammation Cysteine stones usually resistant to ESWL Pass Distal Proximal Uretero-renoscopy ESWL +/- scope Or Perc Nephrolithotomy

Spiral CT of the abdomen/pelvis Observation
A 35-year-old woman is evaluated for a 1-month history of progressive bilateral lower-extremity edema. She was diagnosed with type 1 diabetes mellitus 10 years ago. At her last office visit 4 months ago, the urine albumin-creatinine ratio was 100 mg/g. Medications are enalapril, insulin glargine, insulin aspart, and low-dose aspirin. On physical examination, vital signs are normal except for a blood pressure of 162/90 mm Hg. Cardiopulmonary and funduscopic examinations are normal. There is 3+ pitting edema of the lower extremities to the level of the thighs bilaterally Hgb A1c 7.1%, Albumin 3, Creat 1.1 Urinalysis 3+ protein; 2+ blood; 8-10 dysmorphic RBCs/hpf; 2-5 WBCs/hpf; few RBC casts Urine protein/creat ratio: 5.2mg/mg Kidney ultrasound: R kidney 12.2cm, L kidney 12.7; no hydronephrosis and no kidney masses Which of the following is the most appropriate next step in this patient’s management? Cystoscopy Kidney biopsy Spiral CT of the abdomen/pelvis Observation This patient’s long-standing history of diabetes and proteinuria is suggestive of diabetic nephropathy; however, hematuria and the rapid onset of symptomatic nephrotic syndrome are not consistent with this condition and raise suspicion for primary glomerular disease. Furthermore, patients with diabetic nephropathy often have diabetic retinopathy

Begin training for peritoneal dialysis
A 28-year-old female graduate student with progressive chronic kidney disease due to IgA nephropathy and hypertension is evaluated in the office. She has fistulous Crohn disease for which she has undergone multiple abdominal surgeries, including distal ileum and proximal colon resection as well as a temporary ileostomy and subsequent ileocolic anastomosis. She has been referred to a nephrologist, nutritionist, and social worker and has discussed various methods of kidney replacement therapy, including the risks and benefits. She would prefer kidney transplantation. Medications are lisinopril, calcium acetate, and epoetin alfa. There is no family history of kidney disease. She has type O blood, and her mother and father have blood types B and A, respectively. She has no siblings. On physical examination, temperature is 36.8 °C (98.2 °F), blood pressure is 130/78 mm Hg, pulse rate is 62/min, and respiration rate is 14/min. BMI is 24. Cardiopulmonary examination is normal. Estimated glomerular filtration rate is 23 mL/min/1.73 m2. Which of the following is the most appropriate next step in this patient’s management? Begin training for peritoneal dialysis Evaluate her father as a potential kidney donor Evaluate her mother as a potential kidney donor Plan placement of AV fistula Will likely need HD before a donor is available; PD likely will not work given fistulous Crohn’s disease; parents are not ABO compatible

CKD Common etiologies:
Diabetic: microalbuminuria -> clinical proteinuria -> worsening HTN -> decreased GFR Glomerular Disease: Nephritic vs nephrotic Tubulointerstitial disease (bland UA +/- protein, concentrating defect) Analgesics (NSAIDs), Lead, obstructive nephropathy/chronic reflux Vascular disease Small vessel (SCD, HUS): hematuria, proteinuria Medium vessel (HTN): slow progression Large vessel (RAS) Cystic Disease Transplanted Kidneys Chronic rejection, drug toxicity, recurrence of native disease Stage GFR What to do? 1 >90 Try to slow disease progression 2 60-89 Estimate & try to slow disease progression 3 30-59 Eval & treat disease complications 4 15-29 Prep for RRT 5 <15 (or on HD) RRT

CKD – Associated Complications
Acidosis – Goal: to keep Bicarb 20-26 Uremia – need to be on low-protein diet HTN – Goal: <130/80 Hyperparathyroidism Anemia Renal Osteodystrophy

A 33-year-old woman comes for follow-up examination for a left fibula fracture due to a fall 1 week ago. She has hypertension and stage 5 chronic kidney disease treated with hemodialysis. Medications are lisinopril, sevelamer, epoetin alfa, calcitriol, and kidney vitamins. Exam is normal except for an arteriovenous fistula in the left forearm and a cast on her left leg. Labs: Hgb 10.3, Albumin 3.5, Phos 5.8, Ca 8.4, PTH 700, Alk phos 330 Which of the following is the most likely cause of this patient’s bone disease? Adynamic bone disease Avascular necrosis Osteoporosis Secondary hyperparathyroidism

The dreaded Calcium/Phosphorus balance
Decreased calcium Decreased calcitriol Cholecalciferol (D3) parathyroid Liver PTH 25-hydroxyvitamin D (Calcidiol) Ergocalciferol (D2) X Bone Kidney In CKD, you can’t make calcitriol, so you can’t absorb Ca from intestines – PTH increases as a result, therefore, you start to pull Ca from bones (along with Phos – which builds up in body). You also lose the ability to excrete phos and reabsorp Ca via tubules, so this worsens the problem. Leaving you with elevated phos and putting patient at risk for Calciphylaxis!! *Normal Ca x Phos = 60 X Intestines 1,25-dihydroxyvitamin D (Calcitriol) Increased osteoclast resorption of Ca and Phos X Increased absorption of Ca and Phos Increased Ca resorption; decreased Ca excretion Decreased phos resorption; increased phos excretion CKD: PTH, Phos, calcitriol

Hyperparathyroidism Secondary Hyperparathyroidism
Due to CKD in which PTH is ramped up due to low Ca or calcitriol levels Also leads to hyperphosphatemia Treatment: Calcitriol (1,25-dihydroxyvitamin D) But be warned that this could further elevate Ca and Phos levels (by increasing gut absorption) Keep Ca and Phos wnl (maintain Ca x Phos <55 to avoid calciphylaxis) Avoid phos in diet Phos binders if necessary Calcimimetics (cinacalcet) Only if patient on HD and elevated calcium levels To enhance sensitivity of Ca-sensing receptor to Ca thus blocking further PTH secretion Stop if PTH <150 to prevent adynamic bone disease Tertiary Hyperparathyroidism Results if secondary hyperpara not treated Independent secretion of PTH Treatment: parathyroidectomy

Beta2-microglobuin-associated amyloidosis Osteitis fibrosa cystica
A 59-year-old woman is evaluated for a 2-week history of right hip pain. She has chronic kidney disease treated with peritoneal dialysis. Medications are epoetin alfa, calcium acetate, calcitriol, and a multivitamin. She has no history of exposure to aluminum-containing medications. On physical examination, vital signs are normal. There is tenderness over the right lateral trochanter. Internal and external rotation of the hip elicit pain. Labs: Phos 5.6, Ca 10.2, Alk phos 86, PTH 21, 1,25-dihydroxyvitamin D 52, 25-hydroxyvitamin D 15 Plan radiograph of the right hip shows diffuse osteopenia. An area of lucency is seen along the medial aspect of the femoral neck on the right side consistent with a stress fracture. Which of the following is the most likely cause of this patient’s bone disease? Adynamic bone disease Beta2-microglobuin-associated amyloidosis Osteitis fibrosa cystica Osteomalacia How should you treat this?? Stop Calcitriol and Ca-based binders!!!

Renal Osteodystrophy Osteitis Fibrosa Cystica Osteomalacia
Due to high bone turnover resulting from persistent secondary hyperparthyroidism Elevated PTH, elevated Alk Phos, hyperphosphatemia, hypocalcemia, 1,25-dihydroxyvitamin D deficiency (secondary hyperpara) Xrays: subperiosteal bone reabsorption (esp phalanges, distal clavicles) and areas of sclerosis amidst areas of osteopenia (Rugger Jersey Spine) Can also see areas of rapid osteoclastic activity -> erosive lytic lesions (Brown tumors) that may mimic neoplastic lesions Treatment: same as treating secondary hyperparathyroidism Osteomalacia Low bone turnover disease characterized by increased unmineralized osteoid Due to Vitamin D deficiency and profound hypocalcemia Adynamic Bone Disease Low-turnover (opposite of osteitis fibrosa cystica) Thought to be due to functional hypoparathyroidism due to excess use of vitamin D supplements and/or calcium loading; or after excess removal of functional parathyroid tissue after parathyroidectomy. PTH <100, frequent fractures and bone pain Treatment: discontinuation of Vitamin D analogs and Ca-based binders; stop cinacalcet when PTH <150 Mixed Osteodystrophy – a mix of high and low bone turnover diseases Osteoporosis Often difficult to discern from other osteodystrophies (esp Stage 3-5) – need bone biopsy to prove; use bisphosphonates carefully (renally excreted) DEXA still helpful in Stage 1-2 -> indications for bisphosphonate therapy should mimic general population Amyloidosis (beta2-microglobulin associated amyloid) Deposition into bone can be seen esp in uremic patients who have been on HD for years Xray: cystic bone lesions at the end of long bones

Measure serum erythropoietin Schedule bone marrow examination
A 35-year-old woman with a history of stage 4 chronic kidney disease and hypertension caused by FSGS is evaluated for a 2-month history of fatigue. She has no shortness of breath, melena, or menorrhagia. Medications are lisinopril, low-dose aspirin, sevelamer, and furosemide. On physical examination, vital signs are normal. There is conjunctival pallor. Abdominal examination is normal. A stool specimen is negative for occult blood. Labs: Hgb 8.6, WBCs 5600, MCV 82, Retic count 0.5% of RBCs, Ferritin 25, Transferrin sat 8%, Vitamin B12 600, Folate 15, Creatinine 3.8 Which of the following is the most appropriate next step in this patient’s management? Begin epoetin alfa Begin iron Measure serum erythropoietin Schedule bone marrow examination Iron deficiency anemia (ferritin of 25) should be corrected before initiation of Epo. Iron deficiency: diagnostic if ferritin <100 or transferrin sat <20%

Anemia In CKD, typically due to decreased Epo production
Seen in stage 4 and 5 Anemia of CKD is diagnosis of EXCLUSION No role for measuring Epo levels Erythropoietin-stimulating agents (ESAs) Indications: patients with CKD and Hgb <10 in which other causes of anemia have been excluded NKF-K/DOQI guidelines recommend maintaining Hgb but not exceeding 13 Higher mortality rate, increased cerebrovascular and thrombotic events and HTN Need adequate iron stores (goal transferrin sat >20% and ferritin >100)

Renal Board Review – Part I

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