Case Discussion Nephrology I

Hyperuricemia in STEMI
Patient

Hariogie Putradi

Moderator : Dr. dr. Hani Susianti, Sp. PK (K)

1
 Summary of Data Base
Female, 79 y.o
Anamnesa :
 Chief complaint : Patient suffered from chest pain.
 History of present illness :
˗ Patient has suffered from chest pain since 1 day
before admission, radiating to the back and left arm,
without no activity before pain. The pain did not relieve
with rest or changing position, accompanied by cold
sweat.
˗ She also has shortness of breath since 1 day ago.
˗ Cough (+) since 5 days ago, productive cough with
white sputum, blood (-), night sweating (-).
˗ Fever was denied, Nausea (+) without vomiting. 2
 -She also had little urine production and pain when
urinating.
-Defecation was normal.
 History of past illness :
-Hypertension (+) since 30 years ago. She
routinely consumed adalat oros 30 mg, 1 tab/day.

-Diabetes mellitus (+) since 30 years ago.

She routinely consumed glibenclamide.
-Menopause (+).
 History of family disease :
-Hypertension (+) : his brother.
 Social life :
-She was a housewife, has 2 children.
3
 Physical Examination
Tax: 36°C Weight: 50 kg
HR = 90 Height: 150 cm
BP = 167/90 RR = 22
bpm (normoweight) →
mmHg tpm
regular BMI: 22,22
GA : looked moderately ill GCS 456
Head/
Anemic -/-, ict - Neck = Within normal limits
Neck
Chest Ictus invisible and palpable at ICS V MCL Sinistra
LHM ~ ictus, RHM ~ SL D
Heart: S1, S2 single, murmur-
Lung:
Symetric, percussion s s Rh - - Wh - - V V
ss -- -- V V
ss ++ -- V V
4
 Physical Examination

Abdomen: H/L unpalpable, soefl, bowel sound N

Extremities: edema -/-, warm acral

5
 LABORATORY RESULT
15/08/ 16/08/ 17/08/ 20/08/ Normal
HEMATOLOGY
18 18 18 18 reference
Hemoglobin 12,40 - - 10,90 11,4 – 15,1 g/dL
Erythrocyte 4,32 - - 3,81 4,0 – 5,0.106 /µL
Leukocyte 19,85 - - 8,84 4,7 - 11,3 .103 /µL
Hematocrit 38,30 - - 34,50 38 – 42 %
Thrombocyte 443 - - 320 142 – 424. 103 /µL
MCV 88,70 - - 90,60 80 – 93 fL
MCH 28,70 - - 28,60 27 – 31 pg
MCHC 32,40 - - 31,60 32 – 36 g/dL
RDW 12,30 - - 12,90 11,5-14,5

Diff.count: 0/0/0/ 2/1/0/ 0-4/<1/3-5/

Eo/Baso/Neut/ - -
Lymph/Mono 91/4/5 82/10/5 51-67/25-33/2-5

6
 LABORATORY RESULT
Clinical 15/08/ 16/08/ 17/08/ 20/08/ Normal reference
Chemistry 18 18 18 18
Ureum 81,30 - 59,80 - 16,6 – 48,5 mg/dL
Creatinine 1,26 - 1,16 - <1,2 mg/dL
eGFR 43.54 - 47,9 - mL/min/1,73m2
AST/SGOT 21 - - - 0 – 32 U/L
ALT/SGPT 38 - - - 0 – 33 U/L
RBG 352 - - - < 200 mg/dL
9,50
Equal with mean
Hb-A1c
glucose 226,0 - - - < 5,7%
mg/dL
FBG 284 343 - - 60-100 mg/dL
2HPP BG - 403 - - <130 mg/dL
Uric acid 9,1 - - - 2,4-5,7 mg/dL
7
 LABORATORY RESULT

Clinical 15/08/ 16/08/ 17/08/ 20/08/ Normal reference

Chemistry 18 18 18 18
Total - -
Protein - 5,99 6,7 – 8,7 g/dL

Albumin 3,23 2,91 - - 3,5 – 5,5 g/dL

Globulin - 3,08 - - 2,5-3,5 g/dL
LDH - 1.052 - - 240-480 U/L

8
 LABORATORY RESULT
Cardiac Enzyme 15/08/18 Normal reference

Troponin I 9,80 (09.19.04) Negative <1,0 µg/L

11,10 (14.53.40) Positive ≥1,0 µg/L

CK-MB 26 (09.19.04) 7-25 U/L

45 (14.53.40)
Lipid Profile 15/08/18 Normal reference
Total cholesterol 175 < 200 mg/dL
Trigliserida 336 < 150 mg/dL
HDL 36 > 50 mg/dL
LDL 90 < 100 mg/dL

9
 LABORATORY RESULT

Hemostasis
PPT 15/08/18 Normal reference
Patient 10,30 second 9,4 – 11,3
Control 10,5 second -
INR 0,99 < 1,5
APTT
Patient 26,00 second 24,6 – 30,6
Control 24,9 second -
 LABORATORY RESULT

16/08/ 17/08/ 20/08/ Normal

Electrolyte 15/08/18 reference
18 18 18
Corrected Na: 136 - 145
Natrium 139 - 140 141
143,032 mmol/L
3,5 - 5,0
Kalium 4,87 - 4,52 5,12
mmol/L
98 - 106
Chloride 105 - 103 105
mmol/L

11
Blood Gas Analysis
15/08/18 Result Reference Range
pH 7,26 7,35-7,45
pCO2 56,3 35-45
pO2 149,9 80-100
Bikarbonat 25,4 21-28
(HCO3)
Base Excess -1,9 (-3)-(+3)
O2 Saturation 98,9 >95
Hb 13,0
Suhu 37,0

Conclusion: Respiratory acidosis 12

 Urinalysis 16/08/18 Reference
Clarity Cloudy
Colour Yellow
pH 5,5 4.5 - 8.0
SG 1.025 1.005 - 1.030
Glucose Negative Negative
Protein 2+ Negative
Keton Negative Negative
Bilirubin Negative Negative
Urobilinogen 1+ Negative
Nitrit Negative Negative

13
 Urinalysis 16/08/18 Reference
Leucocyte 3+ Negative
Blood 3+ Negative
Epithel 0,4 ≤ 3 /LPF
Cast Negative
Erythrocyte 294,9 ≤ 3 /HPF
Eumorphic 92%
Dismorphic 8%
Leucocyte 258,5 ≤ 5 /HPF
Crystal Uric acid ++ HPF
Bacteria 15,7 x 103 ≤ 93 x 103 /mL

14
Uric acid crystal

15
 Chest X-Ray (15-08-2018)
Conclusion:
• Cardiomegali
• Pleural effusion Dextra
• Infiltrat (-)

16
 ECG (15-08-2018)

Conclusion:
• Myocardial infarction anteroseptal
17
 Data Interpretation
• Laboratory finding showed leukocytosis with
neutrophilia, elevated RBG, HbA1c, FBG, 2HPP
BG, hyperuricemia, hypoalbuminemia, elevated
troponin I, CKMB, hypertriglyceridemia, negative
glucosuria, proteinuria, hematuria, leukocyturia
without bacteriuria, crystal uric acid, respiratory
acidosis
• Based on medical history, physical examination,
laboratory data & other examinations suggest
STEMI ACS, type 2 DM with Susp. Diabetic
Nephropathy, Sepsis d.t. RTI susp. Pneumoniae
dd. UTI?
18
 Data Interpretation

• Suggestions: Pleural fluid analysis, Urine culture,

Blood culture, Sputum culture, Procalcitonin,
Cystatin C, UACR, Re-urinalysis with special
attention.

• Monitoring: CBC, Total Cholesterol, LDL, HDL,

TG, Troponin I, CKMB, PPT, aPTT, FBG & 2HPP
BG, serum uric acid, Albumin, BGA, ECG, Ureum,
Creatinin, Urinalysis, GFR and SOFA score.

19
• Establishment of Diagnosis
• Hyperuricemia in Myocardial
Infarction and Diabetic
Nephropathy
• Negative glucosuria
• Sepsis

20
 Establishment of Diagnosis
Acute Coronary Syndrome
• Myocardial ischemia is the first step in
developing an myocardial infarction and occurs
as a result of oxygen-supply demand mismatch
or reduced coronary flow.

• The patophysiology underlying ACS is a
atherosclerotic plaque rupture or erosion 
leads to progressive myocardial ischemia
which, if sustained, leads to infarction via 3
possible mechanisms.
Cardiac troponins: from myocardial infarction to chronic disease
Kyung Chan Park, David C Gaze, Paul O Collinson, Michael S Marber
Cardiovascular Research 2017 (113): 1708-1718
21
 Establishment of Diagnosis
Acute Coronary Syndrome
Three possible mechanisms of infarction:
1. intraluminal platelet aggregation resulting in
partial or complete vascular occlusion.
2. release of platelet microaggregates which results
in the microembolization of small vessels to cause
localized ischemia and infarction.
3. progression of white thrombus formation to
clotting-cascade activation which results in partial
or total occlusion of the epicardial artery
Cardiac troponins: from myocardial infarction to chronic disease
Kyung Chan Park, David C Gaze, Paul O Collinson, Michael S Marber
Cardiovascular Research 2017 (113): 1708-1718
22
• Acute Coronary Syndrome

23
 • Acute Coronary Syndrome
ECG in STEMI
Localization of
Infarction
•Septal: V1 and V2
•Anterior: V3 and V4
•Lateral: V5 and V6
•Anteroseptal: V1-V4
•Anterolateral: V3-V6
•Extensive anterior:
V1-V6
•Inferior: II, III, aVF
•High Lateral: I, aVL
•Posterior: tall R wave
and ST depression in
ECG in STEMI Importance and Challenges V1-V2
Rabeea Aboufakher, MD, FACC, FSCAI 24
This patient :
Female, 79 yo
• Troponin I: 9,8 µg/L 11,1 µg/L
• CKMB: 26 U/L  45 U/L
• TG: 336 mg/dL
• HDL: 36 mg/dL
STEMI ACS
• ECG: myocardial infarction
anteroseptal
• Chest X-Ray: cardiomegaly
• chest pain 1 day, radiating to the
back and left arm, cold sweat (+)
• History of HT & DM (+) 30 years

• Monitoring : Total Cholesterol, LDL, HDL, TG,

Troponin I, CKMB, PPT, aPTT, BGA, ECG 25
Diabetic Nephropathy
Patophysiology

26
Diabetic Nephropathy
Patophysiology

27
 Hyperuricemia
• Uric acid is synthesized in the liver from purine
compounds provided by the diet or by the endogenous
pathway of purine synthesis de novo.
• Uric acid then released into the circulation in its soluble
form (monosodium urate), which is readily filtered by the
glomerulus.
• The proximal tubular cells of the kidney reabsorb most of
the uric acid resulting in a normal fractional excretion of
approximately 10%.
• Uric acid accumulation beyond its solubility point (6,8
mg/dL) in water  hyperuricemia

Uric Acid as a Mediator of Diabetic Nephropathy

Diana I. Jalal, David m Maahs, Peter Hovind, Takahiko Nakagawa
Semin Nephrol, 2011 September; 31(5): 459-465
28
Hyperuricemia in Myocardial
Infarction
• Hyperuricemia is often associated with
dyslipidemia, especially hypertriglyceridemia.
• The mechanism of the close relationship between
SUA level and lipid metabolism has not been
understood completely.
• It may involve both metabolic and genetic
defects, which mean lipid metabolic disorders
along with purine metabolic disorders.

Serum uric acid in patients with acute ST-elevation myocardial infarction

Li Chen, Xian-lun Li, Wei Qiao, Zhou Ying, Yan-li Qin, Yong Wang, Yu-jie Zeng, Yuan-nan Ke
World J Emerg Med, Vol 3, No 1, 2012
29
Hyperuricemia in Myocardial
Infarction
• Meanwhile afferent and efferent arterioles of
glomerulus can be involved when lipid metabolic
disorders occur, resulting in the stenosis or
occlusion of arteries and transrenal
excretion of uric acid.
• Uric acid promotes the development of
atherosclerosis, while causing a variety of
cardiovascular events. The possible
mechanisms vary.
Serum uric acid in patients with acute ST-elevation myocardial infarction
Li Chen, Xian-lun Li, Wei Qiao, Zhou Ying, Yan-li Qin, Yong Wang, Yu-jie Zeng, Yuan-nan Ke
World J Emerg Med, Vol 3, No 1, 2012
30
Hyperuricemia in Myocardial
Infarction
• The high level of serum uric acid:
– promotes the oxidation of LDL-C and the peroxidation
of lipid.
– increases the formation of oxygen radicals in
inflammatory reaction.
– increases platelet aggregation and the formation of
uric acid crystals.
• The deposition of uric acid in the arterial wall
could damage the tunica intima of arteries,
promoting coronary thrombosis.
Serum uric acid in patients with acute ST-elevation myocardial infarction
Li Chen, Xian-lun Li, Wei Qiao, Zhou Ying, Yan-li Qin, Yong Wang, Yu-jie Zeng, Yuan-nan Ke
World J Emerg Med, Vol 3, No 1, 2012
31
Hyperuricemia in Diabetic
Nephropathy
• Uric acid has several reported effects by which it
may cause Diabetic Nephropathy, including
endothelial dysfunction, increased activity of
the RAAS, and induction of inflammatory
cascades, in addition to profibrotic cytokine
activation  contribute to progression of
microvascular disease and thereby renal
injury in Diabetic Nephropathy.

Uric Acid as a Mediator of Diabetic Nephropathy

Diana I. Jalal, David m Maahs, Peter Hovind, Takahiko Nakagawa
Semin Nephrol, 2011 September; 31(5): 459-465
32
Hyperuricemia in Diabetic
Nephropathy

Uric Acid as a Mediator of Diabetic Nephropathy

Diana I. Jalal, David m Maahs, Peter Hovind, Takahiko Nakagawa
Semin Nephrol, 2011 September; 31(5): 459-465
33
 Diabetes Mellitus

American Diabetes Association: Standards of Medical Care

in Diabetes-2018 34
Negative Glucosuria

35
Negative Glucosuria
Table 139.1. Substance that may alter tests for glucosuria

Glucosuria 36
STEVEN L. COWART and MAX E. STACHURA
 Salicylic acid: old and new implications for
the treatment of type 2 diabetes?
Negative Glucosuria Graham Rena • Kei Sakamoto
Diabetol Int (2014) 5:212–218

Fig. 2 Schematic illustration of likely antidiabetic targets of salicylate.

Salicylate acts on various cells/tissues. In hepatocytes, salicylate inhibits mitochondrial ATP
production, leading to an increase in AMP/ATP ratio, which stimulates AMPK and also
would be expected to suppress glucose production via multiple inhibitory effects on 37
gluconeogenic pathways.
This patient :
Female, 79 yo Type 2
- Ureum 81,30  59,8
- Creatinine 1,26  1,16
DM with
- eGFR 43,54  47,9 suspect
- Uric acid 9,1 mg/dL Diabetic
- Proteinuria +2, Uric acid crystal ++ Nephro-
- Negative glucosuria pathy
- RBG 352 mg/dL, HbA1c 9,50%
- FBG 284 mg/dL, 2HPP BG 403 mg/dL
- History DM (+) since 30 years ago, routinely
consumed glibenclamide.
- Got ASA (Aspirin) therapy
Suggestion: Cystatin C, UACR
Monitoring : FBG & 2HPP BG, Ureum, creatinine,
urinalysis, GFR 38
149,9/0,95=157,79

443.000

MAP
115,67

GCS 456

Creat 1,26

TOTAL : 4
39
 UTI
Leukocyturia
• A significant number of leukocytes (more than
10,000 per milliliter) is also required for the
diagnosis of urinary tract infection, as it
indicates urothelial inflammation.
• Abundant leukocyturia can originate from the
vagina.
• Bacterial growth without leukocyturia indicates
contamination at sampling.

Urinary Tract Infection. Chapter 7

Alain Meyrier. 40
 UTI

Leukocyturia
• Significant leukocyturia without bacterial
growth (aseptic leukocyturia) can develop
from various causes, among which self-
medication before urinalysis is the most
common.

Urinary Tract Infection. Chapter 7

Alain Meyrier. 41
 UTI
Leukocyturia

Urinary Tract Infection. Chapter 7

Alain Meyrier. 42
This patient :
Female, 79 yo
-Leukocytosis with neutrophilia
Sepsis
-Hypoalbuminemia
d.t.
-UL: cloudy yellow, proteinuria +2,
1. RTI Susp.
leukocyturia +3 without
Pneumoniae
bacteriuria, hematuria +3
2. UTI ?
-SOFA score 4
-Chest X ray: pleural effusion dextra
-Rhonki basal+, SOB 1 day, cough 5
days, white sputum
Suggestion: Pleural fluid analysis, Urine culture, Blood
culture, Sputum culture, Procalcitonin, Re-Urinalysis with
special attention
Monitoring : CBC, Albumin, BGA, and SOFA score
43
 Conclusion
• It has been discussed female 79 y.o with
STEMI ACS, type 2 DM with Susp. Diabetic
Nephropathy, Sepsis d.t. RTI susp.
Pneumoniae dd. UTI?
• Hyperuricemia is often associated with
dyslipidemia, especially hypertriglyceridemia,
and contribute to renal injury in Diabetic
Nephropathy.
• Negative glucosuria may be caused by aspirin
medication.

44
 Conclusion

• Suggestions: Pleural fluid analysis, Urine culture,

Blood culture, Sputum culture, Procalcitonin,
Cystatin C, UACR, Re-urinalysis with special
attention.

• Monitoring: CBC, Total Cholesterol, LDL, HDL,

TG, Troponin I, CKMB, PPT, aPTT, FBG & 2HPP
BG, serum uric acid, Albumin, BGA, ECG, Ureum,
Creatinin, Urinalysis, GFR and SOFA score.

45
THANK YOU

46
No PCCL PL IDx PDx
1 Female, 79 yo Acute STEMI − Monitoring
Coronary ACS Total
syndrome
Cholesterol,
Laboratory Result: LDL,HDL,TG,
• Troponin I: − Monitoring
9,8 µg/L 11,1 Troponin I,
CKMB
µg/L − Monitoring
• CKMB: PPT, aPTT
26 U/L  45 U/L − Monitoring
• TG: 336 mg/dL BGA
− Monitoring
• HDL: 36 mg/dL ECG
ECG: myocardial
infarction
anteroseptal
Chest X-Ray:
cardiomegaly
47
No
PCCL PL IDx PDx
1 Female, 79 yo

Anamnesa:
˗ Chest pain since 1 day
before admission,
radiating to the back and
left arm, without no
activity before pain.
˗ The pain did not relieve
with rest or changing
position, accompanied by
cold sweat.
˗ History of hypertension &
diabetes mellitus 30 years

48
No PCCL PL IDx PDx
2 Female, 79 yo -Type 2 Type 2 - Cystatin C
DM DM with - UACR
Laboratory Result: -Protein- suspect - Monitoring
-Ureum 81,30  59,8 uria Diabetic FBG and
-Creatinine 1,26  1,16 -Hyper- Nephro 2HPP BG
-eGFR 43,54  47,9 uricemia pathy - Monitoring
-Uric acid 9,1 mg/dL with uric
serum uric
-Proteinuria +2 acid
crystal + acid
-Uric acid crystal ++ - Monitoring
+
-Negative glucosuria Ureum,
-RBG 352 mg/dL creatinine,
-HbA1c 9,50% urinalysis
-Equal with mean GFR
glucose 226,0 mg/dL
-FBG 284 mg/dL
-2HPP BG 403 mg/dL
49
No PCCL PL IDx PDx
2 Female, 79 yo

Anamnesa:
-History DM (+) since
30 years ago, routinely
consumed
glibenclamide.
-Got therapy ASA
(aspirin) since August
15th,2018

50
No PCCL PL IDx PDx
3 Female, 79 yo Sepsis Sepsis -Pleural fluid
Laboratory Result: d.t. analysis
-Leukocytosis with 1.RTI -Urine culture
neutrophilia susp -Blood culture
-Hypoalbuminemia 3,23 Pneu- -Sputum
-UL: cloudy yellow, moniae culture
proteinuria +2, 2. UTI? -Procalcitonin
leukocyturia +3, leu -Re-Urinalysis
258,5/HPF with special
hematuria +3, ery attention
294,9/HPF, eumorphic -Monitoring
92%, dismorphic 8% CBC, Albumin
bacteriuria 15,7x103 /mL -Monitoring
SOFA score 4 BGA, SOFA
score

51
No
PCCL PL IDx PDx
3 Female, 79 yo

Chest X-ray: pleural

effusion dextra

Physical examination:
Pulmo: Rh -/-
-/-
+/+
Anamnesa:
˗ shortness of breath since
1 day ago.
˗ Cough (+) since 5 days
ago, productive cough
with white sputum, blood
(-), night sweating (-).
52