BUN stands for blood urea nitrogen. The BUN test is often done to check kidney function. BUN Increases by 10-20 mg/dl/day if renal function absent. Serum creatinine is a better measure of renal function and BUN is reabsorbed at renal tubules [31-33]. Decrease of BUN level may be seen in severe liver disease, malnutrition, and sometimes when a person is overhydrated. A decrease of BUN level may indicate lower risk of kidney disease. BUN-to creatinineratio is considered a reliable test that helps in detecting kidney problems. BUN and creatinine are two compounds found in the blood and the amount of these substances is directly governed by the functioning of the kidneys. The principle behind this ratio is the fact that both urea (BUN) and creatinine are freely filtered by the glomerulus, however urea reabsorbed by the tubules can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption) [31-33]. Any dysfunction of the kidneys can increase or decrease the quantity of these compounds in the blood. In this study, NMB noticeably increase the BUN level and BUN to Creatinineratio. So the drug may have nephrotoxic effect.
CKD classifications is one of the most important kidney function evaluation criteria. GFR is usually determined bymeasuring creatinine in serum and 24 hr urine. Research done in the past has established simple and easy to use online formula for calculating eGFR using serum creatinine value and age of the patient.. Among the three suggested formulae viz MDRD, C-G and CKD-EPI Creatinine 2009, the last one is very easy to use by a small clinical laboratory in an Indian setup. The MDRD formula at times may give ± 10 % variations in values between measured and calculated (1). Although the use of CysC for calculating eGFR will give accurate results, the day to day measurements based on CysC is not feasible for laboratories in developed countries as the reagent for this test is expensive (3). In this study we used the simple CKD-EPI on line calculator as this provides both eGFR as well as CKD category classifications. We did not correlate our findings of eGFR with the measured GFR using serum and urine creatinine values. As the aim of this study was to screen CKD category in patients attending regular check-ups by calculating eGFR , practical measurements were not done. As the MDRD formula is sensitive to assay methodology of creatinine, we preferred to use the CKD-EPI formula (8). As GFR is central to the first line of diagnosis for CKD, we undertook this study to screen patients attending the outpatient clinic to find out if they have any degree of CKD disorders (9). We then classified the % of patients having CKD disorders using the guidelines provided by National Kidney Foundation of USA.We also found out correlation of eGFR to BUN/Creatinineratio and very good correlations were obtained.
in the real world. Indeed, many factors are known to modify BCR independently of effective circulating vo- lume. Gastro intestinal bleeding, a high protein diet, the catabolic effects of fever, trauma, infection, thyrotoxi- cosis, drugs such as tetracycline or corticosteroids, all in- crease protein turnover resulting in increased hepatic production of urea and increase BCR [5, 6]. Conversely, in osmotic diuresis and with the use of acetazolamide, proximal tubular reabsorption of salt and water is im- paired leading to an increase in excreted urea and a decrease in BCR even in states of hypovolemia. BCR also decreases in patients with liver failure or protein malnu- trition due to lower levels of BUN [5, 6]. One can also speculate that AKI is probably due to functional and in- trinsic disease coexisting in different proportions, in a given patient at a given time. Indeed, it is assumed that a continuum exists which leads from prerenal to intrin- sic AKI, the proportion of each changing over time . It can then easily be assumed that BCR would only be reliable if the underlying disease was 100% prerenal or 100% intrinsic, which is probably rarely the case.
ACR- Albumin to creatinineratio; BUN – Blood urea nitrogen; CKD – Chronic Kidney disease; CKD-EPI – Chronic Kidney disease – Epidemiology Collaboration; CKDu – Chronic kidney disease of unknown aetiology; COPCORD – Community acquired program for the control of rheumatic disease; E-GFR – Estimated glomerular filtration rate; ESRD – End stage renal disease; IDMS – Isotope dilution mass spectroscope; JOABPEQ – Japanese orthopaedic association back pain evaluation questionnaire; MDRD – Modification of Diet in Renal disease; MOH – Ministry of Health; NCD – Non-communicable diseases; NCP – North Central Province; NSAID’s – Non-steroidal anti-inflammatory drugs; NWP – North Western Province; WHO – World Health Organization.
The blood samples were subjected to CBC which includes total white blood cell count (tWBC), total red blood cell count (tRBC), haemoglobin (Hb), packed cell volume (PCV), platelet count, mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), mean corpuscular haemo- globin concentration (MCHC); and CS which includes alkaline phosphatase (AP), aspartate ami- notransferase (AST), blood urea nitrogen (BUN), creatinine, glucose, lactate dehydrogenase (LDH), total bilirubin (TBL), total protein (TP), albumin, albumin/globulin (A/G) ratio and to immunoassay for various fractions of globulins (alpha, beta and gamma).
Result of correlation studies which showed in table 2 explain there no correlation between study groups and age, duration. There correlation between study groups and number of cigarette per days has significant value that mean increase number of cigarette per day lead to increase effect of cigarette on albumin creatinineratio.
In this study, urinary calcium/ creatinineratio was lower in women with preeclampsia when compared to Normotensive women. Statistical analysis showed significant correlation of urinary calcium – creatinineratio between women who developed Preeclampsia and Normotensive women with p value of < 0.001. These findings were similar to the studies of Hellen Rodriguez M et al , Ozcan T et.al , Patricia A devine et.al , Das Gupta mandira et al, Kazerooni T et.al , Kar J et.al , Suzuki Y et.al.
Analyzed data on the relationship among patients’ comorbidi- ties, demographic and laboratory data, frailty and pneumonia severity, and the presence of a DNR order are presented in Table 1. Patients in the DNR group were older and tended to have lower levels of protein, albumin, and cholesterol and higher levels of blood urea nitrogen (BUN) and creatinine. The DNR group needed a vasopressor to maintain blood pressure more frequently and had a higher degree of confused consciousness and severe pneumonia, as defined by the PSI score or CURB-65 score. The FI and prevalence of frailty were higher in the DNR group. Concentrations of C-reactive protein or white blood cells and incidences of comorbidity did not differ between the groups.
Preparations were stained with hematoxylin & eosin (routine staining method) and analyzed using an Olympus BX50 binocular light micro- scope at 100 ×, 200 ×, and 400 × magnifica- tion; microphotographs were obtained and evaluated. A scoring system was used to deter- mine the level of renal injury, according to the necrosed cell ratio in the cortical proximal tubu- lar segment, as follows: 0: no necrotic cells; 1: necrotic cell count < 10%; 2: necrotic cell count 10%-25%; 3: necrotic cell count 25%-50%; 4: necrotic cell count > 50%.
Mycobacterium tuberculosis was detected by real-time polymerase chain reaction (rPCR) assay of tracheal lavage fluid. She was diagnosed as having severe ARDS that developed from TB pneumonia. Anti-tuberculous therapy and cardiopulmonary support were started. However, her respiratory condition deteriorated despite treatment with high- frequency oscillating ventilation (HFO), vasopressor support, and 1 g/kg of immunoglobulin. On the third day after admission, her International Society on Thrombosis and Hemostasis DIC score had increased to 5. Recombinant human soluble thrombomodulin (rTM) was administered to treat the DIC. After the administration of rTM was completed, OI gradually decreased, after which the mechanical ventilation mode was changed from HFO to synchronized intermittent mandatory ventilation. The DIC score also gradually decreased. Plasma levels of soluble receptor for advanced glycan end products (sRAGE) and high mobility group box 1 (HMGB-1), which are reported to be associated with ARDS severity, also decreased. In addition, inflammatory biomarkers, including interferon-gamma (IFN- γ ) and interleukin-6 (IL-6), decreased after the administration of rTM. Although severe ARDS (P/F ratio ≦ 100 mmHg) continued for 19 days, the patient ’ s OI and P/F ratio improved gradually, and she was extubated on the 27th day after admission. The severe ARDS with DIC was successfully treated, and she was discharged from hospital on day 33 post-admission.
athy and its possible mechanisms such as anti- oxidant and anti-inflammatory activities. Our results show that administration of ginkgolide B to diabetic rats reduced levels of creatinine and BUN, and volume of 24-urea protein. Creatinine and BUN are considered as markers of kidney lesions, and are increased in rats wi- th diabetic nephropathy [28, 29]. Further, gink- golide B attenuated edema of tubular and glo- merular lesion. These results suggest that gink- golide B ameliorated diabetic nephropathy. Figure 3. Changes of inflammatory response. A. TNF-α level in serum was
Venous blood sample was collected using two tubes. About 2 ml of blood in EDTA tube was used for total WBC analysis using Sysmex 2000i hematology analyzer (Sysmex, Japan). Blood (5 ml) was drawn into serum separator tube (SST) for clinical chemistry tests (uric acid, creatinine, BUN and LDH) using Mindray clinical chemistry analyzer (Shenzhen Mindray Biomedical Elec- tronics, China) and for electrolyte analysis (potassium, sodium, chloride and calcium). This was done before and after chemotherapy; and duration differs based on stage of malignancy. Prophylactic management was done for all admitted patients.
All were evaluated with detailed history, complete systemic examination, Investigations- Hemoglobin (Hb), WBC, Blood Urea Nitrogen (BUN), Serum Creatinine, Serum Electrolytes including calcium, Serum Proteins, Lipid profile, Serum Aluminium, Serum intact PTH assay, Urine routine, Ultrasonography- Kidney, Urter & Bladder (USG-KUB), Electrocardiography (ECG), Two dimensional Echocardiography (2D Echo) and X ray chest. Serum aluminium levels were measured by spectrophotometry. Levels were done in 32 CKD & 32 controls. Aluminum levels in municipal tap water & water post Reverse Osmosis treatment in our centre were measured.
Urimary excretion of hydroxyprolin (Hyp) is one index of total collagen degradation, from all sources. Since some of the Hyp released from collagen may be further metabolized before it is excreted, other markers are necessary to measure collagen breakdown. Excretion of the glycosides of hydroxylysine (Hyl), glucosyl galactosyl hydroxylysine (Hy1[Gl)cGa1]), and galactosyl hydroxylysine (Hyl[Ga)]), more accurately reflects collagen metabolism since these products occur in specificratios in different tissue collagens and are themselves metabolized only to a minor degree. The ratios of total Hy1/Hyp and Hyl(GlcGal)/Hyl(Ga1) were measured in the urine of norma. subjects and of patients with Paget's disease of bone, hyperphosphatasia, and extensive thermal burns. In patients with extensive thermal burns the pattern of urinary Hy1 and its glycosides was consistent with degradation of collagen in dermis and fascia. When bone collagen degradation was dominant, the pattern of urinary metabolites reflected that source. Pagetic bone collagen has an amino acid composition similar to normal bone and Hy1(G1cGa1/Hyl(G1) of 0.396-0.743,vs. normal of 0.474+/- 0.088. In untreated patients with severe Paget's disease of bone or hyperphosphatasia (urinary Hyp greater than 2.0 micronmol/mg creatinine) urinary Hyl/Hyp averaged 0.052+/- 0.042 (0.042+/-0.009 in normal bone) and Hy1(G1cGa1)/Hy1(Ga1) 0.601+/-0.017 (0.47+/- 0.009 in normal bone). When bone resorption was decreased sufficiently with calcitonin or disodium etidronate in these patients, both the urinary ratios of Hy1/Hyp and
This manuscript was aimed to evaluate the antiurolithiatic potential of Parmelia perlata extract (PPE) against calcium oxalate calculi in experimental rats. The drinking water containing 0.75% v/v Ethylene Glycol (EG) and 1% w/v Am- monium Chloride (AC) was used to induce hyperoxaluria in Wistar rats. Thirty-six rats divided into six groups (each containing six animals) were treated with vehicle (Normal control), EG + AC (Urolithiatic control), Cystone (Stan- dard), and 100, 300 and 500 mg/kg, PPE (Tests). Administration of EG + AC produced significant hyperoxaluria and altered biochemical parameters of urine, serum and kidney tissue homogenates in lithiatic group. It caused glomerular atrophy, tubular deposition of oxalate crystals, altered renal architecture and impaired renal functions. PPE (100, 300 and 500 mg/kg, p.o., once daily for four weeks) significantly (p < 0.05) reversed the biochemical changes in urine, serum, and kidney tissue homogenates. It restored the normal renal functions and biochemical parameters like urinary pH, volume, creatinine clearance, BUN levels, uric acid concentrations and some inorganic parameters like oxalate, calcium, phosphorus contents, etc. The histopathological studies revealed that PPE restored the normal renal archi- tecture in lithiatic rats. Conclusively, the experimental findings showed that PPE exhibited significant antiurolithiatic potential against calcium oxalate calculi in experimental rats.
A 3-year-old Arabic boy from Yemen presented with inter- mittent episodes of shortness of breath, lethargy, fatigabil- ity, vomiting, and "cyanotic" discoloration of his skin, lips, mucous membranes and nail beds for the past two years. He was thought to have methemoglobinemia due to persistent cyanosis. He was born in Yemen and moved to the USA for further treatment one year prior to his visit to our clinic. He was evaluated in several institutions in Yemen, Europe and the USA for these problems but no specific diagnosis was ever made. He had one maternal uncle who died suddenly at 35 years of age and 4 full sib- lings (all males) who died of unknown causes between 2 and 4 years of age. His deceased siblings had similar symptoms and discoloration of mucous membranes. None of them had autopsies. He had 4 other siblings (2 brothers and 2 sisters) who were alive with no medical problems. He had normal electrolytes, blood urea nitro- gen (BUN) and creatinine (Cr) levels on several occasions. He had normal results for cardiac examination, echocardi- ogram, hematologic evaluation and hemoglobin electro- phoresis.
The BUN, creatinine, ALT and AST levels were significantly higher in the Endo Group than in the Control Group, and our results suggest that the administration of NAC was sufficient to reduce the extent of hepatic and renal damage caused by endosulfan. Based on the histopath- ological examination of the renal specimens in these groups, renal tissue damage in the Endo Group was observed, and this damage was reversed in the Endo + NAC Group. Prominent cellular damage at both proximal and distal tubular epithelial cells in the NAC Group was thought to have caused the disrupted levels of BUN and creatinine. On the contrary, significant histopathological alteration was observed in the liver tissue of neither the Endo Group nor the Endo + NAC Group.
dium, chloride, BUN, creatinine, and lactate. These vari- ables were chosen for their pervasiveness in and high relevance to intensive care. A total of 29,149 adult ICU admissions were analyzed and missing data were ex- cluded. Because MIMIC II is a fully de-identified public database, the need for informed consent and research ethics review was waived. MIMIC II data were extracted in Oracle SQL Developer (version 3.2.09).
31% (33 of 108 patients) in the COPD group and 8% (six of 73 patients) in the non-COPD group (see Table 3) when evaluated with eGFR Cr , indicating a significantly higher prevalence of CKD in the COPD group (P = 0.0004) with an odds ratio of 4.91 (95% confidence interval, 1.94–12.46, P= 0.0008). When evaluated with eGFR Cys , the prevalence of CKD was 53% (57 of 108 patients) in the COPD group and 15% (eleven of 73 patients) in the non-COPD group, indi- cating a significantly higher prevalence in the COPD group (P,0.0001) with an odds ratio of 6.30 (95% confidence interval, 2.99–13.26, P,0.0001). Note that the prevalence evaluated with eGFR Cys was higher than that evaluated with eGFR Cr . No significant correlation was found between the severity of airflow obstruction and the prevalence of CKD in the COPD group (Table 4).