Transcript Renal Board Review – Part I April 4, 2013 53yo man has a 3 week history of increasing weakness and anorexia.

Renal Board Review – Part I
April 4, 2013
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 350.
What is the most likely cause of this patient’s hyponatremia?
1.
2.
3.
4.
Mineralocorticoid deficiency
Low solute diet
Nephrotic syndrome
SIADH
25%
1
25%
25%
2
3
25%
4
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? 25%
1.
2.
3.
4.
25%
25%
2
3
25%
Glucocorticoid insufficiency
Cerebral salt wasting
Hypothyroidism
Syndrome of inappropriate antidiuretic hormone secretion
1
4
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 118.
Which of the following is the most appropriate next step in this patient’s management?
1.
2.
3.
4.
3% saline infusion
50% glucose by intravenous bolus
Intravenous furosemide
Normal saline infusion
25%
1
25%
25%
2
3
25%
4
Hyponatremia
Plasma Osmolality
Low (<275)
Normal
Check Volume
Status
Hypovolemic
Renal Losses (Una
>20)
Hypervolemic
Euvolemic
Extrarenal Losses
(Una <10)
Appropriately Low
Uosm (<100)
Inappropriately
high Uosm
Nephrotic Sx
Diuretics
Vomiting/Diarrhea
Primary Polydypsia
SIADH
CHF
Mineralocorticoid
insufficiency
Insensible losses
Low solute
diet/Beer
potomania
Hypothyroidism
ESLD
Salt-wasting
nephropathy
Third spacing
(Pancreatitis)
Glucocorticoid
insufficiency
ESRD
Cerebral Salt
Wasting
High (>295)
PseudohypoNa
Mannitol
Isosmotic irrigating
solution
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
• Etiologies:
–
–
–
–
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 24-36 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
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?
1. Adrenal insufficiency
20%
20%
20%
2. Impaired kidney potassium excretion
3. Lactic acidosis
4. Proximal renal tubular acidosis
5. Rhabdomyolysis
1
2
3
20%
4
20%
5
Hyperkalemia
• Etiologies/Mechanisms:
1.
Potassium shifts (from intracellular to extracellular):
– Rhabdo, hemolysis, hyperosmolar states, insulin deficiency, beta-blockers, metabolic
acidosis
2.
3.
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:
1. Potassium shifts (from extracellular to intracellular)
• Inhaled beta-agonists, insulin, hypothermia, excess
catecholamines, metabolic alkalosis
2. Total body depletion (associated with low urine chloride)
• Vomiting, diarrhea
3. 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.
25%
25%
25%
25%
Which of the following is the most likely cause of this
patient’s new findings?
1. Hypercalcemia
2. Hypokalemia
3. Hyponatremia
4. Hypophosphatemia
1
2
3
4
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:
1. Primary disorder?
2. Appropriate Compensation?
3. Anion gap?
4. Delta-delta?
5. Osmolar gap?
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
25%
25%
25%
25%
ABG: 7.33/28/98 on RA
Polarized light microscopy of urine sediment is normal
Which of the following is the most likely diagnosis?
1.
2.
3.
4.
Diabetic nephropathy
Distal (type 1) renal tubular acidosis
Hypertensive nephrosclerosis
Proximal (type 2) renal tubular acidosis
1
2
3
4
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?
25%
25%
25%
1. Alcoholic ketoacidosis
2. Ethylene glycol toxicity
3. Methanol toxicity
4. Salicylate toxicity
1
2
3
25%
4
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?
1.
2.
3.
4.
25%
25%
25%
2
3
25%
Alcoholic ketoacidosis
Methanol poisoning
Ethylene glycol poisoning
Lactic acidosis
1
4
Metabolic Acidosis
• AGMA – MUDPILES
• NAGMA – HARDUP
(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
–
•
Bicarb is excreted -> NAGMA
–
Bicarb usually around 16-18 and VERY difficult to treat with supplemental bicarb
•
•
•
Multiple Myeloma
SC disease
Heavy Metals (wilson’s Lead, Mercury)
Drugs (Ifosfamide)
Acetazolamide
Complications:
–
–
•
PO bicarb rapidly excreted in urine and can’t be reabsorbed
PO bicarb can actually worsen hypokalemia
Causes:
–
–
–
–
–
•
All these are now excreted instead of reabsorbed (Fanconi’s Syndrome)
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
•
•
•
•
•
Causes:
–
–
–
•
Autoimmune (Sjogren’s, SLE)
Drugs (AmphoB, Lithium)
Genetics
Complications:
–
Nephrolithiasis & nephrocalcinosis
•
•
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
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)
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?
1.
2.
3.
4.
5.
Alcoholic ketoacidosis
Diabetic ketoacidosis
Ethylene glycol
Isopropyl alcohol
Toluene
20%
1
20%
20%
2
3
20%
4
20%
5
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
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 6.5-8.0), 1+ blood, no protein, 0-3 RBCs/hpf, no bacteria, no glc
Urine Ca excretion: 230mg/24h (nml 100-300mg/d)
Urine citric acid excretion: 350mg/24h (nml 320-1240mg/d)
Urine oxalate excretion: 140mg/24h (nml 9.7-40.5mg/d)
25%
25%
25%
25%
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?
1.
2.
3.
4.
Begin allopurinol
Begin hydrochlorothiazide
Begin sodium citrate
Increase dietary calcium intake
1
2
3
4
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?
25%
25%
25%
25%
1.
2.
3.
4.
Allopurinol
Hydrochlorothiazide
Potassium citrate
Probenecid
1
2
3
4
Kidney Stones
~1-3%
Kidney Stones
• Calcium Oxalate Stones (~80%)
– 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, 25-50 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
25%
25%
25%
25%
patient?
1.
2.
3.
4.
Extracorporeal shock-wave lithotripsy
Intravenous cephalexin
Intravenous saline
Percutaneous nephrostomy
1
2
3
4
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?
1.
2.
3.
4.
Extracorporeal shock-wave lithotripsy
Intravenous cephalexin
Percutaneous nephrolithotomy
Start potassium citrate
25%
1
25%
25%
2
3
25%
4
Acute
Management
of Kidney
Stones
 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
Symptomatic
Stone
Size of stone
<5mm
>7mm
5-7mm
Hydration
Analgesia
CCB/a-blocker/steroids
Fail to
pass
Locate
stone
Pass
Distal
Ureterorenoscopy
Proximal
ESWL +/- scope
Or
Perc Nephrolithotomy
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?
1.
2.
3.
4.
Cystoscopy
Kidney biopsy
Spiral CT of the abdomen/pelvis
Observation
25%
1
25%
25%
2
3
25%
4
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.
25%
25%
25%
25%
Which of the following is the most appropriate next step in this
patient’s management?
1. Begin training for peritoneal dialysis
2. Evaluate her father as a potential kidney donor
3. Evaluate her mother as a potential kidney donor
4. Plan placement of AV fistula
1
2
3
4
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?
1.
2.
3.
4.
Adynamic bone disease
Avascular necrosis
Osteoporosis
Secondary hyperparathyroidism
25%
1
25%
25%
2
3
25%
4
The dreaded Calcium/Phosphorus
balance
Decreased
calcitriol
Decreased
calcium
Cholecalciferol (D3)
parathyroid
Liver
PTH
25-hydroxyvitamin D (Calcidiol)
X
Bone
Kidney
X
1,25-dihydroxyvitamin D (Calcitriol)
Increased osteoclast resorption
of Ca and Phos
X
Increased Ca resorption; decreased Ca excretion
Decreased phos resorption; increased phos excretion
CKD: PTH,
Ergocalciferol (D2)
Phos, calcitriol
Intestines
X
Increased absorption
of Ca and Phos
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
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?
1.
2.
3.
4.
Adynamic bone disease
Beta2-microglobuin-associated amyloidosis
Osteitis fibrosa cystica
Osteomalacia
25%
1
25%
25%
2
3
25%
4
Renal Osteodystrophy
•
Osteitis Fibrosa Cystica
–
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)
•
–
•
Treatment: same as treating secondary hyperparathyroidism
Osteomalacia
–
Low bone turnover disease characterized by increased unmineralized osteoid
•
•
–
–
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
–
–
•
Due to Vitamin D deficiency and profound hypocalcemia
Adynamic Bone Disease
–
–
•
•
Can also see areas of rapid osteoclastic activity -> erosive lytic lesions (Brown tumors) that may mimic neoplastic lesions
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
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?
1.
2.
3.
4.
Begin epoetin alfa
Begin iron
Measure serum erythropoietin
Schedule bone marrow examination
25%
1
25%
25%
2
3
25%
4
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 11-12
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)