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Internal Medicine Board Review > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Answer these four questions when solving acid-base problems:

A
  1. What is the primary disturbance?
  2. Is compensation appropriate?
  3. What is the anion gap?
  4. Does the change in the anion gap equal the change in the serum bicarbonate concentration (a value called the delta-delta)?
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2
Q

Acidemia

A

pH <7.38

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3
Q

Metabolic acidosis

A

= [HCO3] <24 meq/L

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4
Q

Respiratory acidosis

A

Respiratory acidosis = arterial PCO2 >40 mm Hg.

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5
Q

Alkalemia

A

pH >7.42

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6
Q

Metabolic alkalosis

A

Metabolic alkalosis = [HCO3] >24 meq/L

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7
Q

Respiratory alkalosis

A

Respiratory alkalosis = arterial PCO2 <40 mm Hg.

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8
Q

Metabolic Acidosis Expected Compensation (Acute)

A

Acute: Δ arterial PCO2 = (1.5)[HCO3–] + 8 ± 2

Failure of the arterial PCO2 to decrease to expected value = complicating respiratory acidosis

Excessive decrease of the arterial PCO2 = complicating respiratory alkalosis

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9
Q

Metabolic Acidosis Expected Compensation (Chronic)

A

Chronic: Δ arterial PCO2 = [HCO3–] + 15

Failure of the arterial PCO2 to decrease to expected value = complicating respiratory acidosis

Excessive decrease of the arterial PCO2 = complicating respiratory alkalosis

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10
Q

Respiratory acidosis Expected Compensation (Acute)

A

cute: 1 meq/L ↑ in [HCO3–] for each 10 mm Hg ↑ in arterial PCO2

Failure of the [HCO3–] to increase to the expected value = complicating metabolic acidosis
Excessive increase in [HCO3–] = complicating metabolic alkalosis

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11
Q

Respiratory acidosis Expected Compensation (Chronic)

A

Chronic: 3.5 meq/L ↑ in [HCO3–] for each 10 mm Hg ↑ in arterial PCO2
Failure of the [HCO3–] to increase to the expected value = complicating metabolic acidosis

Excessive increase in [HCO3–] = complicating metabolic alkalosis

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12
Q

Metabolic alkalosis Expected Compensation (Acute)

A

0.7 meq/L ↑ in arterial [HCO3–] for each 1 mm Hg ↑ in PCO2

This response is limited by hypoxemia

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13
Q

Respiratory alkalosis Expected Compensation (Acute)

A

Acute: 2 meq/L ↓ in [HCO3–] for each 10 mm Hg ↓ in arterial PCO2

Failure of the [HCO3–] to decrease to the expected value = complicating metabolic alkalosis
Excessive decrease in [HCO3–] = complicating metabolic acidosis

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14
Q

Respiratory alkalosis Expected Compensation (Chronic)

A

Chronic: 4 meq/L ↓ in [HCO3–] for each 10 mm Hg ↓ in arterial PCO2

Failure of the [HCO3–] to decrease to the expected value = complicating metabolic alkalosis
Excessive decrease in [HCO3–] = complicating metabolic acidosis

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15
Q

Anion Gap

A

anion gap = [Na+] − ([Cl–] + [HCO3–]).

Normal anion gap is 12 ± 2 meq/L

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16
Q

When the primary disturbance is not a metabolic acidosis, the anion gap helps detect

A

“hidden” anion gap metabolic acidosis.

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17
Q

An anion gap (<4 meq/L) suggests

A

multiple myeloma or hypoalbuminemia

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18
Q

Common causes of anion gap acidosis include:

A
  1. DKA
  2. CKD
    l3. actic acidosis (usually due to tissue hypoperfusion)
  3. aspirin toxicity
  4. alcoholic ketosis
  5. methanol and ethylene glycol poisoning
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19
Q

Common causes of normal anion gap metabolic acidosis include:

A

!. GI HCO3– loss (diarrhea)

  1. kidney HCO3– loss (ileal bladder, proximal renal tubular acidosis)
  2. reduced kidney H+ secretion (distal renal tubular acidosis, type IV renal tubular acidosis)
  3. Fanconi syndrome (phosphaturia, glucosuria, uricosuria, aminoaciduria)
  4. carbonic anhydrase inhibitor use
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20
Q

Urine Anion Gap

A

defined as (urine [Na+] + urine [K+]) – urine [Cl–].

UAG is normally between 30 to 50 meq/L

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21
Q

Negative Urine Anion Gap

A

Metabolic acidosis of extrarenal origin is usually suggested by the clinical circumstances but in uncertain cases is suggested by a large negative UAG

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22
Q

Positive Urine Anion Gap

A

metabolic acidosis caused by distal (type 1) renal tubular acidosis, hypoaldosteronism (including type 4 renal tubular acidosis), and CKD.

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23
Q

Delta-Delta

A

in anion gap acidosis, the expected ratio between the change in anion gap and the change in plasma [HCO3] concentration (Δ anion gap/Δ [HCO3]) is 1 to 2.

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24
Q

If (Δ anion gap/Δ [HCO3]) is <1, consider

A

concurrent normal–anion gap acidosis

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25
Q

If (Δ anion gap/Δ [HCO3]) is >2 consider

A

concurrent metabolic alkalosis.

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26
Q

First step in assessing hyponatremia

A

is to classify it as either hyperosmolar or hypo-osmolar

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27
Q

Patients with hyponatremia and hyperosmolality have

A

pseudohyponatremia

In these patients, look for the presence of an osmotically active substance that is confined to the extracellular fluid

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28
Q

Conditions associated with pseudohyponatremia include:

A

hyperlipidemia, hyperproteinemia, and hyperglycemia

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29
Q

If the patient has hypo-osmolar hyponatremia, further classify the hyponatremia based on:

A

the patient’s volume status.

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30
Q

Evaluating Hypo-osmolar Hyponatremia

Hypovolemia (hypotension, tachycardia)

A

Spot urine sodium 20:1
Urine osmolality >450 mosm/L

DDx: GI or kidney fluid losses, dehydration, adrenal insufficiency

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31
Q

Evaluating Hypo-osmolar Hyponatremia

Hypervolemia (edema, ascites)

A

Spot urine sodium 20:1
Urine osmolality >450 mosm/L

DDx: HF, cirrhosis, kidney failure

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32
Q

Evaluating Hypo-osmolar Hyponatremia

Euvolemia (normal volume)

A

Spot urine sodium >20 meq/L
BUN/creatinine 300 mosm/L

DDx SIADH, hypothyroidism

SIADH = syndrome of inappropriate antidiuretic hormone secretion.

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33
Q

Evaluating Hypo-osmolar Hyponatremia

Euvolemia (normal volume)

A

Spot urine sodium >20 meq/L
BUN/creatinine <20:1
Urine osmolality 50-100 mosm/L

Compulsive water drinking

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34
Q

Causes of SIADH include

A

malignancy (small cell lung cancer)

intracranial pathology

pulmonary diseases, especially those that increase intrathoracic pressure and decrease venous return to the heart

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35
Q

medications can cause SIADH, including

A

thiazides, SSRIs, tricyclic antidepressants, narcotics, phenothiazines, and carbamazepine (Tegretol).

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36
Q

DetectAlcohol Poisoning By Calculating the

A

Osmolal Gap = Measured - Calculated osmolality

Normal Osmolal gap is 10 mosm/kg H20; if large gap exists consider alcohol poisoning as the source of unmeasured osmols

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37
Q

Clues for Ingestion of Specific Types of Alcohol

Somnolence or coma and normal acid-base homeostasis

A

Isopropyl alcohol

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38
Q

Clues for Ingestion of Specific Types of Alcohol

Severe anion gap metabolic acidosis and acute visual symptoms or severe abdominal pain

A

Methanol (pancreatitis and retinal toxicity)

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39
Q

Clues for Ingestion of Specific Types of Alcohol

Severe anion gap metabolic acidosis and acute kidney injury

A

Ethylene glycol (metabolizes to glyoxylate and oxalic acid, which may cause calcium oxalate nephrolithiasis and acute kidney injury)

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40
Q

Clues for Ingestion of Specific Types of Alcohol

Anion gap metabolic acidosis and ketoacidosis

A

Ethanol

most common cause of alcohol poisoning

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41
Q

Cerebral salt wasting syndrome causes:

A

hypo-osmolar hyponatremia and laboratory parameters exactly like that of SIADH

Spot urine sodium >20 meq/L
BUN/creatinine 300 mosm/L

associated with hypovolemia, hypotension, and a neurosurgical procedure or subarachnoid hemorrhage within the previous 10 days.

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42
Q

Treatment for hyponatremia due to volume depletion, including hyponatremia from thiazide diuretics and cerebral salt wasting syndrome

A

normal saline

43
Q

Treatment for hypo-osmolar hyponatremia associated with neurologic symptoms:

A

3% hypertonic saline infusion and furosemide to correct the serum sodium to 120 meq/L

44
Q

Treatment for outpatients with SIADH:

A

Fluid restriction is used initially for asymptomatic outpatients with SIADH.

Demeclocycline can also be used for outpatients who do not respond to fluid restriction.

45
Q

In hyponatremic patients, Do not correct the serum sodium faster than:

A

0.5 meq/h (about 12 meq over 24 hours).

46
Q

Vaptan agents should not be used to treat:

A

hypovolemic hyponatremia

The IV V1 and V2 receptor antagonist conivaptan and the oral V2 receptor antagonist tolvaptan (vaptans) are approved for treatment of euvolemic and hypervolemic hyponatremia. Therapy must be initiated in the hospital and is very expensive. No data to date show the vaptans are associated with improved patient outcomes compared with conventional therapy.

47
Q

Hypernatremia (causes)

A

serum sodium >145 meq/L

  1. Defective thirst mechanism
  2. inadequate access to water (older patients in nursing homes)
  3. kidney concentrating defect (DI, most commonly due to lithium)
  4. impaired pituitary secretion of ADH.

Most commonly, hypernatremia is due to loss of hypotonic fluids (GI, kidney, skin) with inadequate water replacement.

48
Q

Most common causes of hyperkalemia include

A
  1. hyporeninemic hypoaldosteronism
  2. acute and chronic kidney failure
  3. low urine flow states
  4. medications (ACE inhibitors, ARBs, potassium-sparing diuretics, pentamidine, trimethoprim-sulfamethoxazole, and cyclosporine)
  5. potassium shifts (rhabdomyolysis, hemolysis, hyperosmolality, insulin deficiency, β-adrenergic blockade, and metabolic acidosis)

Absolute levels of potassium cannot reliably determine if a life-threatening condition exists. Only ECG can assess the effect of hyperkalemia on the cardiac membrane.

49
Q

Significant hyperkalemia associated with a normal ECG suggests:

A

pseudohyperkalemia

50
Q

If hyperkalemia is associated with ECG changes or arrhythmias, begin:

A

IV calcium gluconate to stabilize the myocardium

shift potassium inside the cells with insulin and glucose or inhaled β-adrenergic agonists

removing potassium from the body with oral cation exchange resins, loop diuretics (particularly if volume is overloaded), and dietary potassium restriction

Hemodialysis is often needed to correct life-threatening hyperkalemia but is never the “first step” because of the time delay in initiating dialysis.

51
Q

Most common causes of hypokalemia are:

A

Vomiting and diarrhea (urine [Cl–] <20 meq/L)

Use of diuretics (elevated urine [Cl–]).

52
Q

Characteristic findings in severe hypophosphatemia are:

A

HF, muscle weakness, rhabdomyolysis, hemolytic anemia, and metabolic encephalopathy.

53
Q

Common Causes of Hypophosphatemia:

A
  1. refeeding after starvation
  2. insulin administration for severe hyperglycemia
  3. hungry bone syndrome following parathyroidectomy
  4. respiratory alkalosis
  5. chronic diarrhea
  6. chronic alcoholism
  7. hyperparathyroidism
  8. vitamin D deficiency
54
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:
Minimal proteinuria, no hematuria or pyuria; presence of broad, muddy brown casts

Think of:

A

ATN

And Select:
FENa and/or spot urine sodium

55
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:
Erythrocytes, erythrocyte casts, or dysmorphic erythrocytes

Think of:

A

Glomerulonephritis

And Select as appropriate:

Titers for ANA, anti-dsDNA antibodies, and antistreptolysin O antibodies and C3, C4, and CH50; hepatitis and HIV serologies and cryoglobulins; p-ANCA/c-ANCA and anti-GBM antibodies

56
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Pyuria

Think of:

A

Pyelonephritis, AIN

And Select:
Culture urine
Examine medication list

57
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Livedo reticularis (violaceous reticular rash)

Think of:

A

Cholesterol emboli

And Select:

Look for previous vascular procedure (angiography)
Consider vasculitis

58
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Eosinophilia, eosinophiluria, and rash
Think of:

A

AIN, cholesterol emboli

And Select:

Examine medication list
Look for previous vascular procedure (angiography

59
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Hypercalcemia and anemia

Think of:

A

Multiple myeloma

And Select:
Serum and urine protein electrophoresis, quantitative immunoglobulins

60
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Nephrotic syndrome, urine protein >300 mg/dL

Think of:

A

Diabetes mellitus, renal vein thrombosis

And Select:
Plasma glucose
Renal vein Doppler study

61
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Obstruction on kidney ultrasound

Think of:

A

BPH, nephrolithiasis, obstructing malignant mass, retroperitoneal fibrosis

And Select:
Residual bladder volume, noncontrast CT or MRI

62
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Complete anuria

Think of:

A

Renal cortical necrosis

And Select:

Kidney ultrasonography

63
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Large kidneys on ultrasound

Think of:

A

Amyloidosis, diabetes (early), HIV nephropathy

And Select:

Serum protein electrophoresis, HIV serologic studies, plasma glucose

64
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Kidney failure following colonoscopy

Think of:

A

Phosphate-containing enemas (acute calcium phosphate crystal deposition in the kidneys)

And Select:

Supportive care (fluids, stop ACE inhibitors, ARBs, NSAIDs)

65
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Recent abdominal surgery, hemorrhage or acute pancreatitis

Think of:

A

Abdominal compartment syndrome

And Select:

Intravesicular pressure >20 mm Hg

66
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Peripheral blood smear schistocytes, thrombocytopenia

Think of:

A

Thrombotic microangiopathy (HUS/TTP, DIC, scleroderma renal crisis)

And Select:
As indicated, CBC, coagulation parameters

67
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:

Urine dipstick positive for blood, no erythrocytes on urinalysis

Think of:

A

Hemolysis, rhabdomyolysis

And Select:

Serum CK, serum haptoglobin, reticulocyte count, peripheral blood smear

68
Q

Differential Diagnosis of Acute Kidney Injury - When you see this:
AKI associated with acute leukemia or lymphoma or its treatment

Think of:

A

Tumor lysis syndrome

And Select:

Uric acid, phosphorus, potassium (all elevated)

69
Q

Acute Kidney Injury (AKI) is divided into two categories:

A

oliguric (≤400 mL/24 h) and nonoliguric (>400 mL/24 h) forms.

70
Q

FENa is used to help differentiate:

A

prerenal azotemia from ATN

FENa = ([Urine Na]/[Serum Na] × 100%)

71
Q

FENa =

A

FENa = ([Urine Na]/[Serum Na] × 100%)

72
Q

Interpretation of the FENa in patients with oliguria:

If >1%, consider:

A

ATN or AIN.

Urinalysis will help define the underlying pathology (AIN is associated with leukocytes and leukocyte casts, occasionally with eosinophils).

73
Q

Interpretation of the FENa in patients with oliguria:

If <10 meq/L) and urinalysis is benign, consider

A

prerenal azotemia

74
Q

Interpretation of the FENa in patients with oliguria:

If <10 meq/L) and urinalysis shows erythrocytes, dysmorphic erythrocytes, and erythrocyte casts or proteinuria, consider

A

glomerulonephritis

75
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hypertension
Select:

A

An ACE inhibitor or ARB; use a loop diuretic rather than a thiazide for GFR <30 mL/min/1.73m2

Examples loop diuretics
Furosemide
Bumetanide

76
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Serum protein-creatinine ratio ≥200 mg/mg
Select:

A

Titrate ACE inhibitor and ARB to achieve minimal proteinuria even if patient is normotensive

77
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hemoglobin A1c >7%
Select:

A

More intensive intervention to maintain hemoglobin A1c <7%

78
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Anemia
Select:

A

Erythropoietin to maintain hemoglobin levels of 10-11 g/dL and iron to maintain iron stores (always check iron levels before starting erythropoietin)

79
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Hypocalcemia, hyperphosphatemia
Select:

A

Phosphate binders (calcium acetate, calcium carbonate, sevelamer) to maintain [PO4] between 3.5-5.5 mg/dL

cinacalcet, a calcimimetic, is approved for treatment of secondary hyperparathyroidism in dialysis patients

80
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Metabolic acidosis
Select:

A

Alkali therapy to maintain [HCO3] between 20-26 meq/L

81
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Lipids
Select:

A

Statin therapy to reduce LDL cholesterol <100 mg/dL

82
Q

Drug Therapy for Chronic Kidney Disease (CKD)
If you see this:
Vitamin D deficiency
Select:

A

Calcitriol (or vitamin D analogues)

83
Q

Loop diuretics

A

Furosemide

Bumetanide (much more potent)

84
Q

DDx Chronic Kidney Disease

A 
Diabetes
Glomerular disease
Tubulointerstitial disease
Vascular disease
Structural disease
85
Q

Features and chronic kidney disease caused by:

Diabetic kidney disease

A

Look for early microalbuminuria (spot albumin-creatinine ratio, 30-300 mg/g), followed by overt proteinuria, declining GFR, and a bland urine sediment. The presence of retinopathy strongly suggests coexisting diabetic nephropathy.

86
Q

Features and chronic kidney disease caused by:

Glomerular disease

A

lomerular hematuria, proteinuria, and hypertension, often with other systemic manifestations (lupus nephritis and postinfectious glomerulonephritis)

If nephrotic syndrome is present, look for focal segmental glomerulosclerosis, membranous nephropathy, minimal change disease, and amyloidosis.

kidney biopsy is often needed to make a specific diagnosis and guide therapy.

87
Q

Features and chronic kidney disease caused by:

Tubulointerstitial disease

A

Look for proteinuria, glycosuria, concentrating defect, sterile pyuria, and leukocyte casts, as well as papillary necrosis on ultrasound

Consider analgesic nephropathy (medication use, papillary necrosis), infection (TB, legionnaires disease, leptospirosis), allergic drug reaction (eosinophilia, eosinophiluria), autoimmune disorder (SLE, sarcoidosis, Sjögren syndrome), and lead nephropathy (occupational exposure).

88
Q

Features and chronic kidney disease caused by:

Vascular disease

A

Look for hematuria, proteinuria, and associated systemic illness.

Vasculitis often presents with rapidly progressive glomerulonephritis and palpable purpura (leukocytoclastic vasculitis).

89
Q

Features and chronic kidney disease seen after kidney transplantation:

A

chronic allograft nephropathy, drug toxicity (cyclosporine), polyomavirus BK infection, or recurrence of disease

90
Q

Features and chronic kidney disease caused by:

Structural disease (polycystic kidney disease)

A

Look for hypertension, hematuria, palpable kidneys (advanced disease), family history of CKD.

91
Q

Nephrotic Syndrome

A

Proteinuria (>3.5 g/24 h), hypoalbuminemia, and edema

Other findings may include hyperlipidemia with lipiduria (“Maltese cross” fat droplets in urine seen with polarized light microscopy)

Massive proteinuria results in loss of anticoagulant proteins C and S and places the patient at risk for venous thromboembolism.

92
Q

Causes of Acute Glomerulonephritis

A

Acute poststreptococcal glomerulonephritis

IgA nephropathy

Idiopathic membranoproliferative glomerulonephritis (MPGN)

Secondary MPGN

ANCA-associated glomerulonephritis (prototype is granulomatosis with polyangiitis [Wegener granulomatosis])

Anti-GBM antibody disease (Goodpasture disease)

Cryoglobulinemia

93
Q

Clinical Features of:

Acute poststreptococcal glomerulonephritis

A

** Hematuria occurs 1-3 weeks after sore throat. **

Serum complement levels are low, and anti-DNAse B assay is positive.

Kidney biopsy shows crescents, subepithelial deposits (humps), and mesangial deposits on electron microscopy.

94
Q

Clinical Features of:

IgA nephropathy

A

*** Hematuria occurs 1-2 days after a sore throat. **

Clinical manifestations range from asymptomatic microscopic hematuria to acute or chronic kidney failure.
IgA deposits are present on the immunofluorescence staining of the kidney biopsy.

95
Q

Clinical Features of:

Idiopathic membranoproliferative glomerulonephritis (MPGN)

A

Hypocomplementemia, thickened capillary loops on light microscopy, and immune deposits are seen on electron microscopy.

96
Q

Clinical Features of:

Secondary membranoproliferative glomerulonephritis (MPGN)

A

MPGN is seen in the setting of a chronic infection (HCV, syphilis, endocarditis, HIV), systemic disease (diabetes mellitus, RA), drugs (NSAIDs, penicillamine), and solid tumors (breast, colon, lung, kidney).

97
Q

Clinical Features of:

ANCA-associated glomerulonephritis (prototype is granulomatosis with polyangiitis [Wegener granulomatosis])

A

Nasal congestion, ulceration, chronic sinusitis, and/or pulmonary (often nodular) infiltrates are found.
Pathologic findings include a proliferative glomerulonephritis in the setting of positive c-ANCA or p-ANCA.

98
Q

Clinical Features of:

Anti-GBM antibody disease (Goodpasture disease)

A

Glomerulonephritis and pulmonary hemorrhage are present.

Linear staining of the GBM seen on immunofluorescence microscopy.

99
Q

Clinical Features of:

Cryoglobulinemia

A

Palpable purpura, arthritis, neuropathy, and digital ischemia are present.
Low complement levels and cryoglobulins are present in the serum or on kidney biopsy specimens.
Can be associated with HCV.

100
Q

If you see this…
Pulmonary infiltrates or nodules, sinusitis, nasal ulcers, saddle nose deformity, or glomerulonephritis

Think this…

A

Granulomatosis with polyangiitis (Wegener granulomatosis)

** Nearly 95% of patients with granulomatosis with polyangiitis have sinus disease. The absence of sinus disease rules out this disorder.**

Choose this …

c-ANCA, p-ANCA, and antiproteinase-3 (anti-PR3)

101
Q

If you see this…
Glomerulonephritis and alveolar hemorrhage

Think this…

A

Anti-GBM antibody disease (Goodpasture disease)

Choose this …

Anti-GBM antibodies; immunofluorescence microscopy revealing linear staining of IgG lining the GBM

102
Q

If you see this…
Pulmonary hemorrhage, nephritis, arthralgia, serositis, rash, anemia, thrombocytopenia, leukopenia

Think this…

A

SLE

Choose this …

Anti-dsDNA or anti-Sm antibodies

103
Q

If you see this…
Bacterial endocarditis or cryoglobulinemia

Think this…

A

Immune complex-mediated disorders

Choose this …

Serum cryoglobulins and blood cultures

104
Q

Important risk factors for kidney stone formation include:

A
  1. insufficient fluid intake
  2. increased dietary sodium and protein intake
  3. hypercalciuria, hyperuricemia, hyperoxaluria
  4. low urine citrate levels (citrate inhibits crystal formation)
  5. primary hyperparathyroidism with hypercalciuria
  6. metabolic syndrome and type 2 diabetes mellitus
  7. recurrent UTIs with urease-splitting organisms such as Klebsiella and Proteus (struvite stones)

Internal Medicine Board Review (1 decks)

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