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  1. Hashim OH, Shuib AS, Chua CT
    Nephron, 2001 Dec;89(4):422-5.
    PMID: 11721160
    We have studied the interaction of the Gal-GalNAc-reactive champedak lectin-C with neuraminidase-treated and untreated IgA1 from IgA nephropathy patients. The binding ability of the lectin to untreated IgA1 from IgA nephropathy patients was significantly lower as compared to the untreated IgA1 from normal controls. This differential lectin-binding capacity was abrogated when the experiment was performed on neuraminidase-treated sera. Treatment of the serum IgA1 with neuraminidase also abrogated the differential charge distribution between the alpha-heavy chains of IgA nephropathy patients and normal controls.
  2. Shuib AS, Chua CT, Hashim OH
    Nephron, 1998;78(3):290-5.
    PMID: 9546689
    Sera of IgA nephropathy (IgAN) patients and normal subjects were analysed by two-dimensional (2-D) gel electrophoresis. Densitometric analysis of the 2-D gels of IgAN patients and normal subjects revealed that their protein maps were comparable. There was no shift of pI values in the major alpha-heavy chain spots. However, the volume of the alpha-heavy chain bands were differently distributed. Distribution was significantly lower at the anionic region in IgAN patients (mean anionic:cationic ratio of 1.184 +/- 0.311) as compared to normal healthy controls (mean anionic:cationic ratio of 2.139 +/- 0.538). Our data are in support of the previously reported findings that IgA1 of IgAN patients were lacking in sialic acid residues.
  3. Ho LM, Cheong I, Jalil HA
    Nephron, 1996;72(4):676-8.
    PMID: 8730441
    The latex of pokok ipoh (Antiaris toxocaria) and the root bark of akar ipoh (Strychnos species) have been the main sources of the poisonous principles in dart and arrow poisons prepared throughout south-east Asia. We report a fatal case of rhabdomyolysis and acute oliguric renal failure following oral ingestion of blowpipe dart poison. To our knowledge this is the first such report.
  4. Segasothy M, Abdul Samad S, Zulfiqar A, Shaariah W, Morad Z, Prasad Menon S
    Nephron, 1994;66(1):62-6.
    PMID: 8107955
    Computed tomography (CT) and ultrasonography (US) were performed in 40 patients who had consumed excessive quantities of analgesics (> 1 kg) to compare their value in the diagnosis of analgesic nephropathy (AN). The computed tomography and sonographic features were renal papillary calcifications. Renal papillary necrosis (RPN) was documented in 20 of 40 patients by US and in 14 of 40 patients by CT. In 11 patients, both US and CT were positive. In 9 patients, US was positive whilst CT was negative. In 3 patients, CT was positive whilst US was negative. Prevalence of RPN was 50% using US and 35% using CT. Using US as a gold standard, sensitivity of CT was 55%, specificity 85%, positive predictive value 78.6% and negative predictive value 34.6%. Percent agreement with CT and US was 70%. Cohen's kappa statistic adjusting for chance agreement was 40%. Based on these results, it is found that US yielded a higher percentage of positive cases of RPN.
  5. Segasothy M, Suleiman AB, Puvaneswary M, Rohana A
    Nephron, 1988;50(1):50-4.
    PMID: 3050572
    180 patients with end-stage renal disease (ESRD) on maintenance dialysis and those who had undergone renal transplantation were questioned retrospectively. 14 patients had consumed excessive quantities of analgesics (greater than 1 kg) prior to the institution of long-term dialysis or transplantation. Sonographic examination done on these patients indicated that 7 had renal papillary necrosis (RPN). The sonographic features were renal papillary calcifications surrounding the central sinus in a complete or incomplete garland pattern. In 5 of these patients RPN is attibutable to the excessive consumption of paracetamol. We have earlier reported 10 cases of RPN due to excessive consumption of paracetamol. Thus 15 cases of RPN attributable to paracetamol consumption (1.0-15.3 kg over a period ranging from 3 to 23 years) have been documented. It is concluded that paracetamol may assume an increasingly important role in the causation of analgesic nephropathy (AN) and ESRD.
  6. Mohd Tahir NA, Mohd Saffian S, Islahudin FH, Abdul Gafor AH, Othman H, Abdul Manan H, et al.
    Nephron, 2020;144(4):204-212.
    PMID: 32050196 DOI: 10.1159/000505296
    BACKGROUND/AIMS: G73A polymorphism in the CST3 gene of cystatin C has been associated with Alzheimer's disease, age-related macular degeneration, and cardiovascular disease. However, studies investigating the influence of this genetic variability on serum cystatin C and cystatin-based renal function estimate are limited. Therefore, the aim of this study is to investigate the possible association of single-nucleotide polymorphism (rs1064039) of the CST3 gene on the serum cystatin C level and cystatin C-based estimated glomerular filtration rate (eGFR).

    METHODS: Study subjects include patients with various levels of renal function recruited from the nephrology clinic and wards of a tertiary hospital. The blood samples collected were analyzed for serum cystatin C and creatinine levels by particle-enhanced turbidimetric immunoassay and kinetic alkaline picrate method, respectively. DNA was extracted using a commercially available kit. -Polymerase chain reaction results were confirmed by direct DNA Sanger sequencing.

    RESULTS: The genotype percentage (G/G = 73%, G/A = 24.1%, and A/A = 2.9%) adhere to the Hardy-Weinberg equilibrium. The dominant allele found in our population was CST3 73G allele (85%). The regression lines' slope of serum cystatin C against creatinine and cystatin C-based eGFR against creatinine-based eGFR, between G and A allele groups, showed a statistically significant difference (z-score = 3.457, p < 0.001 and z-score = 2.158, p = 0.015, respectively). Patients with A allele had a lower serum cystatin C level when the values were extrapolated at a fixed serum creatinine value, suggesting the influence of genetic factor.

    CONCLUSION: Presence of CST3 gene G73A polymorphism affects serum cystatin C levels.

  7. Hian CK, Lee CL, Thomas W
    Nephron, 2016;134(2):59-63.
    PMID: 27476173 DOI: 10.1159/000448296
    Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic disease characterised by the formation of multiple renal cysts that adversely affect renal function. ADPKD shows significant progression with age when complications due to hypertension are most significant. The activation of the renin-angiotensin-aldosterone system (RAAS) occurs in progressive kidney disease leading to hypertension. The RAAS system may also contribute to ADPKD progression by stimulating signalling pathways in the renal cyst cells to promote growth and deregulate epithelial transport. This mini review focuses on the contribution of the RAAS system to renal cyst enlargement and the potential for antagonists of the RAAS system to suppress cyst enlargement as well as control ADPKD-associated hypertension.
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