Reference Interval SI Units

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Natural Ways to Treat Thrombocytopenia

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These data appeared to rule out pancreatitis or a coagulation disorder. Although hemoglobin and hematocrit appeared to have stabilized, thrombocytopenia persisted, and hemolytic anemia remained a possibility. By the second day, however, the patient had virtually no urine output. The following table shows his laboratory results for days 2 and 3:

Analyte

Second Day, am

Second Day, pm

Third Day, am

Urea nitrogen

22 mg/dL

35 mg/dL

42 mg/dL

(7.9 mmol/L)

(12.5 mmol/L)

(15.0 mmol/L)

Creatinine

2.1 mg/dL

3.6 mg/dL

4.4 mg/dL

(186 mmol/L)

(318 mmol/L)

(389 mmol/L)

Hemoglobin

11.6 g/dL

10.5 g/dL

10.6 g/dL

(7.20 mmol/L)

(6.52 mmol/L)

(6.58 mmol/L)

Hematocrit

34% (0.34)

31% (0.31)

31% (0.31)

Platelet count

54 x 103/mL

51 x 103/mL

51 x 103/mL

(54 x 109/L)

(51 x 109/L)

(51 x 109/L)

Magnesium

1.6 mg/dL (0.66 mmol/L)

Peripheral

Unremarkable

Unremarkable

blood smear

Coagulation

Within normal

studies

limits

Reticulocyte

1.8%

count,

corrected

Urinalysis

Within normal

Leukocytes, 1 -5/

limits

Sodium, urine Osmolality, limits hpf; erythrocytes, 5-10/hpf; renal tubular epithelial cells, 1-5/hpf 44 mmol/L 258 mOsm/kg

Rapid rise in serum levels of urea nitrogen and creatinine and developing stability of hemoglobin, hematocrit, and thrombocyte values, together with barely elevated reticulocyte count, turned attention away from the hematological findings and focused it on acute renal failure.

Several consulting physicians, including a clinical pathologist, were called to see the patient. One consultant raised the question of thrombotic thrombocytopenic purpura (TTP)

and the possibility of plasma exchange. A second consultant thought that acute renal failure secondary to acute tubular necrosis (ATN) was more likely and that anemia and thrombocytopenia were probably due to marrow suppression secondary to the infectious process. The pathologist also felt that TTP was unlikely and thus recommended against plasma exchange.

The morning of the next day, the fourth hospital day, the following laboratory studies indicated relatively stable hematological findings and a further increase in serum urea nitrogen and creatinine:

Analyte

Urea nitrogen Creatinine Urea nitrogen/ creatinine ratio (calculated) Hemoglobin Hematocrit Platelet count

Value, Conventional Units

67 x 103/mL

Reference Interval, Conventional Units

14-18 40-54 150- 450

Value, SI Units

67 x 109/L

Reference Interval, SI Units

Dialysis was started, and laboratory results reported on the fifth day were as follows:

Analyte

Hemoglobin Hematocrit Platelet count Bilirubin, total Haptoglobin

Value, Conventional Units

94 x 103/mL 0.6 mg/dL Within normal limits

Reference Interval, Conventional Units

Value, SI Units

94 x 109/L 10 mmol/L

Reference Interval, SI Units

Over the next several days the hematological picture improved spontaneously; hemoglobin rose to 12 g/dL (7.45 mmol/L), hematocrit to 36% (0.36), and platelet count to 191 x 103/mL (191 x 109/mL). Serum electrolytes, acid-base values, and urea nitrogen, determined during this period of hemodialysis, stabilized. A disintegrinlike and metallopro-teinase domain with thrombospondin Motifs-13 (ADAMTS-13) enzyme level performed by a reference laboratory was normal, ruling out TTP. The patient remained in acute renal failure until the 22nd hospital day when urine output increased to 500-1000 mL/d. Renal biopsy performed on the 22nd hospital day showed regenerating tubules consistent with improving ATN. By the 27th hospital day, urine output was > 1500 mL/day, and serum urea nitrogen and creatinine were decreasing without further dialysis. When serum potassium fell to 3.1 mmol/L, oral potassium supplementation was initiated. After an uneventful diuretic phase, the patient was discharged with only medications for his hypertension.

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