The hereditary forms of polycystic kidney disease of autosomal dominant PKD (ADPKD) and autosomal recessive PKD (ARPKD) are the main forms. ADPKD is a multifactorial disorder characterized by bilateral renal cysts and commonly affects adult patients. The most common extrarenal manifestations of ADPKD are liver cysts and is often incidental findings and clinically insignificant. A case report has been reported with polycystic disease in the kidneys and liver with autoimmune hemolytic anemia. ADPKD is a progressive disease and symptoms tend to get worse over time. ADPKD involves managing the symptoms and slowing disease progression. The most serious complication of ADPKD is end stage kidney failure. This aim of this study were to determine the symptoms and laboratory tests that confirm the diagnosis of polycystic kidney disease accompanied by autoimmune hemolytic anemia.
AbstrakPenyakit Ginjal Kronik (PGK) adalah kelainan struktural atau fungsi yang terjadi lebih dari 3 bulan dan mempunyai implikasi terhadap kesehatan serta diklasifikasikan berdasarkan penyebab, laju flitrasi glomerulus (LFG) dan albuminuria. Komplikasi serius yang ditimbulkan PGK dapat berupa malnutrisi, kelebihan cairan, perdarahan, serositis, depresi, gangguan kognitif, neuropati perifer, infertilitas dan Infeksi. Untuk mencegah komplikasi tersebut, diperlukan indikasi dan waktu yang tepat untuk memulai terapi dialisis pada pasien PGK. AbstractChronic Kidney Disease (CKD) is a structural or functional abnormality that occurs more than 3 months and has health implications and is classified based on causes, glomerular filtration rate (GFR) and albuminuria. Serious complications caused by CKD can include malnutrition, excess fluid, bleeding, serositis, depression, cognitive impairment, peripheral neuropathy, infertility and infection. To prevent these complications, it is necessary to indicate and the right time to start dialysis therapy in CKD patients.
AbstrakSepsis didefinisikan sebagai infeksi bersama dengan manifestasi sistemik dari infeksi. Sepsis berat adalah penyebab 50% kasus acute kidney injury (AKI) pada pasien kritis. Patofisiologi cedera ginjal akut (AKI) pada sepsis disebabkan oleh respon inflamasi, toksin dan perubahan hemodinamik glomerulus. Tingkat keparahan disfungsi ginjal tergantung pada tingkat keparahan sepsis. Perubahan laju filtrasi glomerulus (GFR) adalah fenomena AKI yang terlambat. Diagnosis AKI dengan mengukur kreatinin serum. Sayangnya, kreatinin adalah indikator yang kurang dapat diandalkan selama perubahan akut pada fungsi ginjal. Munculnya penanda biologis baru dalam lingkup AKI sangat membantu bagi dokter untuk dapat mendiagnosa awal AKI. Penanda biologis AKI bisa menjadi komponen serum atau urin. Penanda biologis urin menjanjikan untuk mendeteksi awal AKI, sehingga dapat berguna untuk diagnosis dini. Abstract Sepsis is defined as infection along with systemic manifestations of infection. Severe sepsis is the cause of 50% of acute kidney injury (AKI) cases in critical patients. Pathophysiology of acute kidney injury (AKI) in sepsis is caused by inflammatory response, toxin and changes in glomerular hemodynamics. The severity of renal dysfunction depends on the severity of sepsis. Changes in glomerular filtration rate (GFR) are a late phenomenon of AKI.Diagnosis of AKI by measuring serum creatinine. Unfortunately, creatinine is a less reliable indicator during acute changes in kidney function. The emergence of new biological markers within the scope of AKI is very helpful for clinicians to be able to diagnose early AKI. Biological markers of AKI can be a component of serum or urine. Urine biological markers are promising to detect early AKI, so it can be useful for early diagnosis.
<p><em>Asidosis tubular renal (ATR) merupakan tubulopati ginjal yang jarang terjadi, dimana terdapat ketidakmampuan ginjal untuk menjaga perbedaan pH normal antara darah dan lumen tubulus ginjal. Pada kondisi ini terjadi gangguan pengasaman urin disebabkan gangguan reabsorbsi bikarbonat, gangguan ekskresi ion hidrogen, atau keduanya sehingga mengakibatkan asidosis metabolik. ATR ditandai dengan adanya asidosis metabolik dengan senjang anion plasma yang normal, hiperkloremik dan laju filtrasi glomerulus normal. ATR terbagi menjadi 3 tipe utama, yaitu ATR tipe 1 (ATR distal), tipe-2 (ATR proksimal), dan tipe 4 (ATR hiperkalemia). ATR distal merupakan ATR yang disebabkan oleh defek pada tubulus distal ginjal, dimana defek ini menyebabkan gangguan pada sekresi ion hidrogen. Beberapa penelitian menunjukkan bahwa ATR tipe 1 dikaitkan dengan mutasi genetik. Mutasi genetik herediter dapat autosomal dominan atau autosomal resesif. Gambaran klinis dapat mencakup kelainan pertumbuhan tulang, kelemahan atau kelumpuhan otot, deposit kalsium di ginjal, anoreksia, muntah, konstipasi, diare, dehidrasi, dan poliuria. Telah dilaporkan kasus pasien wanita usia 19 tahun dengan keluhan utama kelemahan di kedua tangan dan kaki. Dari penelusuran klinis dan laboratorium didapatkan hipokalemia dan berdasarkan pendekatan hipokalemia dengan HCO3- rendah dan pH urine >5,5, diagnosis pada pasien ini ditegakkan sebagai asidosis tubulus renal distal (ATRd).</em></p><p><strong><em>Kata kunci:</em></strong><em> </em><em>ATR, ATRd, asidosis metabolik, hiperkloremik, hipokalemia </em><em></em></p><p><strong><em>Abstract</em></strong></p><p><em>Renal tubular acidosis (RTA) is a condition caused by the inability of the kidneys to maintain normal pH differences between the blood and tubules lumen of the kidney. Renal tubular acidosis is a rare kidney tubulopathy. In this condition, urine acidification is caused by bicarbonate reabsorption, disruption of hydrogen ion excretion, or both, resulting in metabolic acidosis. RTA is characterized by metabolic acidosis with normal plasma anion, hyperchloremic gaps and normal glomerular filtration rates. RTA is divided into 3 main types, namely type 1 RTA (distal RTA), type-2 (proximal RTA), and type 4 (hyperkalemia RTA). Distal RTA caused by defects in the distal tubules of the kidney, where these defects cause interference with the hydrogen ion secretion. Several studies have shown that type 1 RTA is associated with genetic mutations. Hereditary genetic mutations can be autosomal dominant or autosomal recessive. Clinical features can include bone growth disorders, muscle weakness or paralysis, calcium deposits in the kidneys, anorexia, vomiting, constipation, diarrhea, dehydration, and polyuria. There has been a reported case of a 19-year-old female patient with a chief complaint weakness in both hands and feet. From clinical and laboratory investigations, it was found that hypopotassium and based on the hypokalemia approach with low HCO3- and urine pH >5,5, the diagnosis in this patient was established as a distal renal tubular acidosis (RTAd)</em> <strong><em> </em></strong></p><p><strong><em>Keywords: </em></strong><em>RTA, RTAd ,metabolic acidosis, hypopotassium, hiperchloremic</em></p><p><em> </em></p>
BACKGROUND: The increase in the elderly poses problems in the areas of health, since it can cause aging of the physiological function of organs. It also has an impact on kidney function, which will enhance the chronic kidney disease. One of the theory that causes aging process is the free radical theory, which that accumulation of free radicals is caused by depletion of antioxidants. Therefore, exogenous antioxidants are needed and in this study author use dadih. Dadih is fermented buffalo milk, indigenous from West Sumatera-Indonesia. Peptides found in fermented milk contained antioxidant that can stimulate the formation of endogenous antioxidants and diversification of dadiah increases its effect as antioxidant. AIM: This study aims to prove the effect of dadih antioxidants on malondialdehyde (MDA) levels of kidney tissue and renal interstitial fibrosis. MATERIALS AND METHODS: An experimental study with post-test only control group design conducted to observe effect of dadih to kidney aging of Rattus norvegicus in the Laboratory of Andalas University. It used 30 R. norvegicus which were divided into three groups. Group K was a positive control (did not get dadih), Group P1 was given dadih 4.5 g once a day, and Group P2 was given dadih 4.5 g twice a day for 42 days. After that, MDA levels of kidney tissue are examined using the thiobarbituric acid reactive substances examination technique and examination of renal interstitial fibrosis which is done by histopathology with Sirius-red staining. Data were analyzed using the normality test with Shapiro–Wilk. RESULTS: The results showed that dadih can reduce levels of MDA in kidney tissue, where its decrease very significant in Group P1 (given dadih once a day) and Group P2 (given dadih twice a day) compared to the Group K (control group) 0.97 ± 0.06 pg/ml to 0.75 ± 0.03 pg/ml (p < 0.05). Group P1 and Group P2 can also reduce the renal interstitial fibrosis rank. Obtained a decrease in the average fibrosis rank from Group K to Group P1 and subsequently to Group P2 (p < 0.05). CONCLUSION: This study concluded that dadih can reduce MDA levels in kidney tissue and reduce renal interstitial fibrosis rank on aging kidney.
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