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"Patogenesis nefropati diabetik (ND) merupakan hasil interaksi faktor hemodinamik, metabolik dan lingkungan serta faktor genetik. ND biasanya tidak terdeteksi secara klinis sampai terjadi kerusakan ginjal yang bermakna dapat berupa glomerulosklerosis, tubular atrofi dan fibrosis interstitial. KIM-1 dapat digunakan sebagai penanda adanya kerusakan tubulus ginjal. Hubungan polimorfisme gen ACE dengan nefropati diabetes masih tidak konsisten. Penelitian ini merupakan studi cross sectional komparasi antara dua kelompok penyandang DMT2 dengan atau tanpa nefropati yang bertujuan untuk mengetahui adanya kerusakan tubulus, polimorfisme gen ACE dan menganalisis hubungannya dengan kadar KIM-1 terhadap terjadinya kelainan tubulus. Didapatkan adanya peningkatan ekskresi KIM-1 urin pada 19 subjek pre-nefropati dengan median 1,3 (interquartile 1,5) ng/mL, 25 subjek nefropati insipien dengan median 1,6 (interquartile 2,3) ng/mL dan 12 subjek nefropati overt dengan rerata kadar KIM-1 3,1 ± 2,4 ng/mL. Terdapat polimorfisme gen ACE pada penyandang DMT2. Proporsi genotipe DD 9,3%, ID 33,3% dan II 57,4% pada kelompok NND, pada kelompok ND proporsi genotipe DD 4,7%, ID 34,1% dan genotipe II 61,2%. Dijumpai adanya hubungan bermakna antara alel D dengan peningkatan ekskresi KIM-1 urin pada kelompok pre-nefropati (p = 0,030). Peningkatan kadar KIM-1 urin pada kelompok pre-nefropati menunjukkan adanya kerusakan tubulus yang merupakan proses awal nefropati DM. Distribusi genotipe polimorfisme gen ACE pada penelitian ini menyerupai penelitian lain di negara-negara Asia, sedangkan di negara Eropa genotipe DD lebih banyak daripada genotipe II. Hubungan bermakna alel D dengan kadar KIM-1 hanya pada kelompok prenefropati mungkin disebabkan adanya faktor lain seperti kadar glukosa, kontrol glikemik, ureum, kreatinin dan kadar trigliserida yang memengaruhi. Simpulan: Terdapat peningkatan ekskresi KIM-1 urin pada penyandang DMT2 kelompok pre-nefropati yang meningkat secara bermakna pada penyandang DMT2 dengan nefropati overt. Peningkatan ekskresi KIM-1 urin dapat dipakai sebagai penanda kerusakan tubulus. Terdapat polimofisme gen ACE pada penyandang DMT2. Genotipe II lebih banyak dibanding genotipe ID dan DD. Dijumpai adanya hubungan alel D dengan peningkatan kadar KIM-1 urin pada penyandang DMT2 pre-nefropati.

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The pathogenesis of nephropathy diabetic (ND) is the result of the interaction of haemodynamic, metabolic, environment, and genetic factors. In general, ND was clinically undetectable until kidney has been damaged significantly, in the form of glomerulosclerosis, tubular atrophy, or interstitial fibrosis. KIM-1 can be used as the initial indicator of kidney tubules damage. The relationship between ACE gene polymorphism and diabetic nephropathy was still inconsistent.

This research was a comparative cross-sectional study on two groups of DMT2 patients with and without nephropathy diabetic. The objectives of this study were to identify the tubules damage, ACE gene polymorphism, and to analyze the relationship between the degree of KIM-1 and the tubules damage. The increase of KIM-1 urine excretion was found in 19 pre-nephropathy subject (median = 1.3 with interquartile 1.5 ng/mL), in 25 incipient nephropathy subject (median = 1.6 (2.3) ng/mL), in 12 overt nephropathy subject (Mean = 3.1 ± 2,4 ng/mL). ACE polymorphism gene was found in DMT2 patients. In the NDD group, the genotype proportion of DD = 9.3%, ID = 33.3% and II = 57.4%. Whereas, in the ND group, the figures were 4.7%, 34.1% and 61.2%, respectively.

Significant relationship was found between allele D and the increase of KIM-1 urine on pre-nephropathy group (p = 0.030). The increase of KIM-1 urine on prenephropathy group shows the tubules damage which is the initial process of nephropathy diabetic. The genotype distribution of ACE gene polymorphism in this study was similar with the studies in Asian countries; however, in European countries the genotype DD is found higher than genotype II. The significant relationship between allele D and KIM-1 level in pre-nephropathy group might be the influence of other factors, such as glucose level, glycaemic control, urea, creatinine, and triglyceride level.

Conclusion: There was KIM-1 excretion increased on DMT2 pre-nephropathy group, which increase significantly in DMT2 overt nephropathy group. The increase of KIM-1 urine excretion can be used as the indicator of tubules damage. ACE gene polymorphism was found in DMT2 group, with genotype II was higher than genotype ID and DD. A significant relationship between allele D and the increase of KIM-1 urine excretion was found in pre-nephropathy group."

"Kebocoran plasma sistemik pada sepsis dapat mengakibatkan berbagai komplikasi dari renjatan sampai kematian. Belum ada teknik andal untuk menilai kebocoran plasma sistemik pada anak. Degradasi glikokaliks, ditandai meningkatnya sindekan-1 dalam darah, menyebabkan perubahan permeabilitas vaskular sistemik. Pada glomerulus bermanifestasi sebagai albuminuria sehingga kenaikan rasio albumin-kreatinin (ACR) urin berpotensi menggambarkan kebocoran plasma sistemik. Sampai saat ini belum ada rujukan nilai sindekan-1 dan ACR urin sebagai penanda kebocoran plasma sistemik pada anak. Penelitian ini bertujuan untuk mengetahui peran ACR urin dan nilai rujukan ACR urin sebagai penanda kebocoran plasma sistemik pada anak sepsis dan mengkaji kaitannya dengan sindekan-1.Penelitian ini terdiri atas studi deskriptif pada anak sehat dan penelitian longitudinal prospektif dengan rancangan potong lintang berulang terhadap anak sepsis, dilakukan di RSUP Cipto Mangunkusumo Jakarta, RSUP H. Adam Malik Medan dan RSUP Kariadi Semarang dalam rentang waktu Maret–Desember 2015. Dilakukan pemeriksaan sindekan-1 dan ACR urin pada pasien sepsis yang dirawat di instalasi rawat intensif anak pada hari rawatan ke-1, 2, 3 dan 7, dan mencatat skor Pediatric Logistic Organ Dysfunction pada hari rawatan ke-1 dan 3.Tiga puluh subjek sehat dan 49 subjek sepsis diikutsertakan dalam penelitian. Pada kelompok sehat didapati median ACR urin 10,5 (3–88) mg/g dan rerata sindekan-1 sebesar 27,7 (SB 2,24) ng/mL. Sindekan-1 di atas persentil 90 (41,42 ng/mL) ditetapkan sebagai batasan kebocoran plasma sistemik. Didapati 40 orang (81,6%) subjek sepsis dengan sindekan-1 > 41,42 ng/mL dan 33 orang (67,3%) menunjukkan ACR urin > 300 mg/g pada hari rawatan 1. Didapati koefisien korelasi (r) 0,32 (P < 0,001) antara ACR urin dan sindekan-1. Area under the curve ACR urin terhadap kebocoran plasma sistemik diperoleh sebesar 65,7% (95% IK 54,5–77%; P = 0,012). ACR urin > 157,5 mg/g ditetapkan sebagai cut-off point kebocoran plasma sistemik dengan sensitivitas 77,4% dan spesifisitas 48%. ACR urin dapat digunakan sebagai penanda kebocoran plasma sistemik, peningkatan ACR urin akan mengikuti peningkatan sindekan-1.

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Systemic plasma leakage during sepsis can cause several complications from shock to death. There is no feasible measurement of systemic plasma leakage in children. Glycocalyx degradation, marked by increased serum syndecan-1, alters vascular permeability. In the glomerulus this can manifest as albuminuria, therefore elevated urinary albumin-creatinine ratio (ACR) potentially provides an index of systemic plasma leakage. Nowadays. there is no reference value of syndecan-1 and urinary ACR as a marker of systemic plasma leakage in pediatric population. This study aims to analyze the role of urinary ACR and to determine its reference value as a marker of systemic plasma leakage in pediatric sepsis, by analyzing its correlation with syndecan-1.

This study consisted of descriptive study on healthy children and longitudinal prospective study with repeated cross-sectional design on septic children, was conducted at Cipto Mangunkusumo Hospital Jakarta, Haji Adam Malik Hospital Medan and Kariadi Hospital Semarang from March to December 2015. We examined serum syndecan-1 and urinary ACR of septic patients in pediatric intensive care unit on day 1, 2, 3 and 7. Pediatric Logistic Organ Dysfunction (PELOD) score were recorded on day 1 and 3.

Thirty healthy subjects and 49 septic subjects were recruited. In the healthy group, median of urinary ACR was 10.5 (3–88) mg/g and mean of syndecan-1 was 27.7 + 2.24) ng/mL. Syndecan-1 more than 90th percentile (41.42 ng/mL) was determined as systemic plasma leakage. Forty (81.6%) septic subjects had syndecan-1 > 41.42 ng/mL and 33 (67.3%) subjects had urinary ACR > 300 mg/g on day 1. Correlation coefficient (r) between urinary ACR and syndecan-1 was 0.32 (P < 0.001). Area under the curve of urinary ACR and plasma leakage was 65.7% (95% CI 54.5–77%; p = 0.012). Urinary ACR > 157.5 mg/g was determined as cut-off point of systemic plasma leakage with sensitivity 77.4% and specificity 48%. Urinary ACR can be used as marker of systemic plasma leakage. Increased urinary ACR would indicate increased syndecan-1."