Questions related to Clinical Nephrology
I am preparing to conduct a study to investigate the association between periodontal status and Kidney health in Saudi patients.
Is it logic to examine randomly selected patients in dental clinics (with unknown systemic diseases) to check periodontal health (1st variable), and then send the patients to nephrology unit to check kidney health (second variable)?
A young patient attempted suicide by taking 63 tabs of carbamazepine 200 mg. she was managed with CRRT - CVVH and discharged 10 days later well and couscous.
data supporting the use of hemodialysis in managing carbamazepine poisoning is increasing, so I am not sure if it is worth publishing or not ( if it has a chance to get accepted for publishing)
Does this report indicate any malignancy and what are your recommendations based on these reports?
Transrectal Ultrasonography of the pelvis report:
The prostate is enlarged weighing about 85 gm with apparently intact capsule. The median lobe is hypertrophied indenting the bladder base and mildly projecting within its lumen. Heterogenous parenchymal echogenicity is noted however no definite evidences of focal lesions...BPH...For correlation with PSA level.
Both seminal vesicles are bulky showing tiny cystic changes.
Past Abdomen and Pelvis US report:
Mild circumferential wall thickening of the urinary bladder, with prominent trabeculations and with echofree lumen and no mural lesions..features of chronic obstruction uropathy...for clinical and lab correlation.
Full volume= 315 cc3
Post-voiding volume= 20 cc3
The prostate is enlarged in size (70 cc) seen identing the bladder base with prominent median lobe with intact capsule
Normal size and echogenicity of both seminal vesicles
53 Y F has 3rd degree uterine prolapse associated with bladder prolapse (Will under hysterectomy) but there are some urological problems that arose on examination. Initially Right grade 2 Hydronephrosis on US scan (Abdomen and Pelvic), thus she did CT scan to know the cause as directed by the Urologist and the findings are presented as follow (Image attached - CT image). So my Q is how would you manage the renal stones, Kinks, angiomyolipoma, Hydronephrosis? Will you just observe/wait and see the results after hysterectomy or you will try the ureter stent?
Atrial Fibrillation (Bisoprolol 2.5 mg once daily)
Chronic venous insufficiency (Daflon 500 mg one tablet daily)
Allergic Rhinitis (Cetirizine 10 mg once daily)
Non-Alcoholic Fatty liver disease
The Kidney (Brenner and Rector eds. )
Oxford Textbook of Clinical Nephrology (Davison et al. eds. )
Therapy of Renal Diseases and Related Disorders (Suki and Massry eds. )
Clinical Physiology of Acid-base and Electrolyte Disorders (Burton Rose ed.)
Replacemrnt of Renal Function by Dialysis (Drukker et al. eds.)
Why do almost all the guidelines (WHO) choose urinary iodine to define iodine deficiency but not blood iodine?
I have a group of subjects on supplement A for 3 years. Their blood pressure (BP) and kidney function, as measured by creatinine clearance (eGFR) were monitored at 1-, 2- and 3-year. In unadjusted models, BP decreased and eGFR increased significantly over time. It is well regonised that those who has a better kidney function (higer eGFR) will have a lower BP.
I would like to assess whether the changes in BP remained significant after controlling eGFR (to evaluate whether supplement A has direct effect on BP reduction or indirectly through eGFR improvement). Is it appropriate to use LMM with time-varying covariate for such analysis?
#edit: part of my text went missing earlier
Looking for some information on the effect of high intensity exercise on serum creatinine levels and potential false positive eGFR results?
I'm also interested if an individual with increased muscle mass would effect the serum creatinine levels and eGFR?
I am conducting a research in drug-induced nephrotoxicity. In your opinion, what would be the most suitable standard to define drug-induced nephrotoxicity case? Is it KDIGO Clinical Practice Guideline for AKI or NCI-CTCAE v4.0? Or maybe you have another preference.
Please see the attachment for more details.
The question is addressing the use of SGLT2 inhibitors in a T2DM patient with past history of renal transplant provided his or her eGFR>60 and there are no other contraindications. Please state:
Is there any trial evidence for efficacy and safety?
Do you have any personal experience?
Would you dare do it (personal view)?
creatinine increased up to 4 milligrams in 5 days after IV contrast and starting hydration and antioxidant treatmnet
I have some incomplete data regarding creatinine in mouse urine that I would like to use to evaluate proteinuria. I would like to know what is the usual quantity of creatinine found in 24h urine to compare it to my results, does anyone know it?
During research in urolithiasis, my team has found a few apparently healthy adults with extreme (>50%) variation in creatinine excretion, compared day and night 12-hour sample (from the same day). Obviously, we suspected inadequate collection with >12 hours in the sample with higher creatinine excretion, but those volunteers insisted in a correct collection and seemed to be reliable. The volume excretion was also quite higher in the sample with more creatinine, which was the diurnal one.
Thus, we have been thinking about alternative explanations. We have thought of a possible creatinine clearance variance. Water and other fluids overload should not change significantly glomerular filtration, as this could be usually managed by ADH supression and urine dilution in a rapid way (unless >10 litres/day, which does not seem likely). Protein overload is a well-known cause of increased glomerular filtration, in clinical and experimental settings. But could this be enough for such a different creatinine excretion in a day?
I am conducting a meta-analysis for renal function as outcome. On of them is albuminruia/proteinuria. Some studies have reported albumnuria while other have reported proteinuria. Can I combine both in same meta-analysis?
Some books say ACE inhibitors are contraindicated in renal failure while some say they are first line for treatment of renal failure..I wanna know if they are indicated in renal failure when GFR is going down and creatinine is rising up whats the underlying mechanism by which they improve renal failure.?
I am trying to impute a continuous variable prior to running logistic regression and having trouble with it. Multiple imputation of the continuous variable works perfectly, however, when I categorize it, after imputation but prior to adding to the logistic model, somehow my results change. It appears to be significant loss of power for some reason such that my highly significant variable falls out of significance. For instance, when trying to impute blood sugar values and then running a logistic model against a binary outcome, the parameter estimates are very comparable for all covariates including blood sugar with or without imputed data. However, when I categorize the blood sugar into 4 categories in the imputed dataset and then run it, the variable falls out of significance. If I run the logistic model excluding patients with missing value (pre-imputation) with blood sugar categories, I get very plausible, logical results (comparable to results from an entirely different dataset). Is it wrong to categorize the imputed variable in the imputed dataset?
Hello. I have a population of 500 subjects with 100 cases of MGUS. I would calculate the rate of cases over population among age-class (e.g. 20-29, 30-39, 40-49 etc). My problem is that these cases have been gathered during a follow-up of 14 years. Should I divide population in age -class of 14 years? Thanks.
A 84 year old woman with hypertension, 2 type diabetes mellitus and chronic renal failure (GFR 30-50 ml).
2005 NSTEMI: LAD and LCX PCI
2006 angina pectoris: distal RCA PCI. LAD and LCX stents no changes
2014 UA: RCA ISR. 1 BMS implantation. Other stents without ISR
Echocardiographia all the time showed good systolic ejection fraction with good wall motions.
In 2014 starts: in ECHO showed a non siginificant pericardial effusion. After coronarographia seen hematuria and anemia.
An urological examination was negative for tumor, but an pelvis CT was done, whith some negative result.
2014.07 gastroscopia: duodenitis erosiva and chronic erosive gastritis was.
2015.08.03-04 was admited with melena. Gastroscopy and colonoscopy was not showed a point of bleeding. 3 U of blood was transfused.
An echo showed a significant pericardial effusion and a pericardiocentesis was performed. 1200 cc. straw-yellow liquid evacuated. And other day 100 cc.
2015.08.05-12 admited to hospital with anemia for blood transfusion. Colonoscopy was done again. The source of bleeding was not found. A polyp of the Bauchin valve was cut of.
The histology result of the colonoscopy sample not confirmed malignancy.
2016.01.05 Admited agin with huge pericardial effusion and symptoms of HF. 1500 cc straw-yellow liquid evacuated. A pleural effusion was this time and a diagnostic thoracocentesis was done.
The results from the pleural fluid showed a sigillocellulare cc. cells
The CA 125 was elevetad. (95 the normla range upper limit is 35 at our lab)
Pericardial fluid: eosinophil cells, mesothel and lymphoid cells was seen.
An cardiac MR was done with negative result for a autoimmune disease or primer cardiac malignancy.
An chest CT was done: negative for cc.
An abdominal and pelvis MR was done: at the point of obturator in both side an 6 mm diameter lymphaticus nodus was detected. In the corpus of uterus an 8 mm myoma detected (T2)
The hemoculture results is negative
2016.04.20 was admited with huge pericardial effusion. 1200 cc bloody liquid was evacuated.
And now 2016.05.31. Again was admited with effort dyspnoe and not a very huge pericardial effusion.
The pericardial effusion sizes was 30-35 mm mostly left side and 25 mm from apex and right side.
The gastroentereologist, onkologist, gynecologist and urologyst do not know the reason of chronic pericardial effusion. Please help, what is the diagnostic option which can use to find the cause of pericardial effusion.
Thank you that you read and help.
I often find it challenging to clear patients with ESRD to proceed with renal transplant who also have asymptomatic moderate degree of aortic stenosis (which could progress to severe/critical AS within unpredictable period of time while awaiting for renal transplant).
1): Shall we clear those patients for renal transplant since they have acceptable surgical risks?
2): What are the possible clinical outcomes or best management strategy in case those patients became symptomatic from severe/critical AS within 1-2 years after renal transplant?
Any experience or suggestion?
The patients with chronic renal failure have to undergo hemodialysis. These patients usually have AV fistula. The question is if the blood can be collected from this AV fistula on the beginning, during or after the end of hemodialysis in order to avoid further puncture of vein. I suppose that values like mineralogram or pH will be completely different between these two approaches. But what about drug levels? Does anyone know any study dealing with this issue?
We are injecting collagenase NB8 to the pancrease,
17 minutes in 37 bath,
Filter the suspension through a 425um diameter wire mesh
Use Histopaque to seperate the cells
and wash twice.
Do self sedimentation 6 times..
and yield only 300 islets.
How can I improve the method?
Most of the patients with chronic renal failure suffer from a decline in the level of the hormone Erythropoietin. Are there cases where the hormone levels rise in patients with renal failure? and whether research supports this opinion?? and why this increase there?
I hope the physiological explanation for this phenomenon
In studies monitoring tenofovir-associated kidney impairment either in HIV-positive patients on ART or negative patients on PrEP, a common test is serum creatinine levels, which are used to estimate glomerular filtration rate (GFR). However, some studies have shown that an alternative, cystatin C estimated GFR is more closely associated chronic kidneys disease outcomes. What is the state of the science for most accurately monitoring kidney function in patients on ART or PrEP? Thanks.
patients with tx glomerulopathy have been seen commonly recently. management of tx glomerulopathy is diffucult.
HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.
Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.
CECT is one of the most frequently performed radiological investigations in emergency settings. Though, unquestionably, in certain circumstances, the benefit of CECT outweighs the risk of CIN in patients at risk. However, in all patients where CECT may be helpful should not form a basis for routine practice. The nephrology residents often just act to "clear" the patient for contrast study without actually knowing the patients' condition (save S.ur/ S.cr levels!). The standard line written is CECT may be undertaken if clinically indicated.
The Roche Ketorolac Package insert for Toradol tablets and the ketorolac package inserts from generic manufacturers state that ketorolac is contraindicated in advanced renal impairment, but the degree of renal dysfunction is not specified (i.e. moderate or severe), and specific values for serum creatinine or creatinine clearance are not given. Hospira Medical Information states that the package insert only states “advanced renal failure” as a contraindication, and the degree of renal dysfunction (i.e. moderate or severe) is left to the discretion of the clinician. Drug references such as the Lexicomp Drug Information Handbook and others interpret this as meaning that ketorolac is only contraindicated in severe renal failure, and can be dosed in moderate renal failure at the reduced dose of IV or IM 15mg q6hrs.
A middle aged man presented with nephrotic syndrome (>10 gm protein/24hrs with sev dyslipidemia) with severe thrombocytopenia of almost one year duration. His auto immune profiles are negative, renal biopsy could not be done because of sev thrombocytopenis (Plat 5000). He was started on steroid (Pulse solumedrol follwed by oral prednisone), but there was no improvement. Any suggestion regarding further evaluation and management?
60 year old man presented with chronic renal failure and hyperurecemia but he developed allergy to allopurinol.
Serum creat.= 2.6 mg/dL
Serum uric acid= 9.4 mg/dL
What will be you plan of management?
I am trying to measure Beta-2-Microglobulin concentration in urine samples from patient with renal disease, so the concentration is expected to be high. I first used abcam SimpleStep ELISA kit then R&D Quantikine to confirm. But the inter-assay variation is so big (>100%) leaving me no idea which is the right result. Can anyone suggest how to make these result more reproducible and reliable? Thanks
Attached is some of the results on a spreadsheet.
I have a 15yo girl with HD dependent ESRD over the last 2 years. We don’t know her underlying diagnosis, but we think she has Wegener's. She has no symptoms, other than pos p and c anca antibodies and recurrent severe jaw pain. A recent bone biopsy has just shown chronic inflammation, kidney biopsy at presentation showed 90% globally sclerosed glomeruli.
We were planning to list her for a renal tx last month, but she got very sick. We now know she had macrophage activation syndrome (ferritin 40000) and she has responded well to high dose steroids. Our Rheumatologist thinks it is her underlying autoimmune dz that provoked the macrophage activation, as her bone marrow biopsy is without signs of malignancy and she is EBV negative.
We are now trying to find someone with experience in doing solid organ tx after macrophage activation syndrome. How should we treat the macrophage activation syndrome, and when is she safe to undergo Tx?
We can’t seem to find anything in the literature.
Schaeffner ES, Ebert N, Delanaye P, Frei U, Gaedeke J, Jakob O, Kuhlmann MK, Schuchardt M, TÃ¶lle M, Ziebig R, van der Giet M, Martus P. Two novel equations to estimate kidney function in persons aged 70 years or older. Ann Intern Med. 2012 Oct 2;157(7):471-81
when an eGFR is 15 - 29 ml/min/1.73 m2 which part of treatment, either clinical action alone or Nutrition part- is really works to get back to 30-59 ml/min/1.73 m2 or the actions for preceding stages? or increase the ca absorption, lipoprotein activity or develop the metabolic consequences?
Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
I have a patient with active ankylosing spondylitis(AS) and second (2007;2012) kidney transplantation (due to chronic glomerulonephritis). Ankylosing spondylitis is active with BASDAI . 5,5 - 6,0 during last 3 years, CRO changes from 11 - 25 mg/l (normal value 0 - 5 mg/l), spine ligament calcification has found in 3 cervical and lumbar spine ligaments on X- ray. Due to kidney transplantation the patient use MMF and prednisolone.
Several studies indicated urine flow and Bowman's capsular space were increased/dilated in diabetic nephropathy. Is it possible that the Bowman's capsular space declined in severe diabetic nephopathy (because mesangiolysis, tuft-capsule adhesion or hyalinosis) while urine flow remains high?
We have managed 2 cases. Both of them were diagnosed with SSNS at two years, responded to prednisolone, subsequently became steroid resistant, managed with methylprednisolone and cyclosporine. After stopping cyclosporine a recent relapse shows serum creatinine levels of 3 mg/dl. What should we do?
I need some guides or protocols related to the topic , included some parameters such as ; mesangial matrix expansion, glomerulosclerosis, tuft-to-capsule adhesions, hyalionosis( glomerular or tubular) , dilatation of urinary space and thickening basement membrane of bowman's capsule (light microscopy assessment)
19 YRS,Male.Confirmed MCGN on biopsy,now in CKD 5 stage.His 2 Male,first cousins have renal failure(Children of his mothers 2 sisters) and on dialysis.
Is this an X-Linked inheritance pattern
Can his mother be a kidney donor for him.
I am specifically looking for the interarrival times used for patients/kidneys in KSIM, as well as the resulting probabilities of transplant, death on wait list, and average time spent waiting. I know the the data came from the Organ Procurement and Transplant Network, but this data can only be retrieved through a request process. Is there another place online or in another publication where this information is more easily accessible?
Conference Paper Characteristics of a simulation model of the national kidney...
The use of pre-blood fluid in the reduction of filter clotting in dialysis is well known, but it is also known to reduce the efficiency of the dialysis abilities.
Could you please explain how your unit overcomes the drawback of the use of pre-blood fluid, and how the use of Filtration Fraction determines the use of pre-blood fluid? Some units determine that pre-blood fluid is not needed if the Filtration Fraction is below 30%.
Does this not then save the unit money if pre-blood fluid is not used? Also, it has been stated that in the use of Heparin in Dialysis, the APTT is irrelevant in the ability to stop the filter clotting off. What APTT therapeutic range does your unit run at?
Any information provided would be appreciated.
Some patients with flank pain showed hydronephrosis in sonograghy and IVP, which can be due to UPJO. But in their EC-renal scan they may show non obstructive pattern. Some physicians choose follow up but others perform pyeloplasty.
The result of clinical studies suggested that statins appear to decrease the rate of reduction of estimated glomerular filtration rate (eGFR) and slow the progression of pathologic proteinuria moderately.
For the past two or three weeks, we've noted a number of cases of vascular access bleeding after dialysis. The dose of the anticoagulant used not changed.
What are the possible and common reasons for this?
I'm skeptical, especially as I have refereed a lot of low quality research. However, a conversation with a colleague led me to think that there may be some niche (maybe AKI or research in certain parts of the world?) not currently covered by journals. What do you think? Are there particular forms (e.g. online only, with discussion forums etc.) that you think could enhance nephrology journals?
Hypernatremic dehydration in exclusively breastfed newborns is a problem. Is it exclusively because of inadequate lactation counselling? Do some mother/baby duos also run a risk of hypernatremia despite proper lactational care? Or can this be totally abolished by good lactational counselling?
Usually the ACEI should be discontinued weeks befor performing LDL Apheresis.
Do somebody have information about the danger of anaphylaxy whit Immunoadsorbers when ACEI are used by the patient?
Thank you all.
Although the advent of direct acting antivirals in the management of HCV are evolving such that they do not use interferons, technically these are not indicated for patients with renal failure, due to lack of clearance of metabolites. What experience is there in using them to clear HCV in patients awaiting kidney transplantation? Are these metabolites cleared by hemodialysis? There is a pilot study of sofosbuvir and ribavirin in genotype 1 or 3 hepatitis C virus infected patients who have chronic renal insufficiency (http://clinicaltrials.gov/ct2/show/NCT01958281?term=sofosbuvir+kidney&rank=1).
And how it would be prevented or managed if it happened? And is it usual that it happened each session? Attach references if available.
What are the last KDOQI guidelines for dialysate bicarbonate concentration?
Are there any limits? Or is the only recommendation pre-dialysis serum concentration of bicarbonate > 22 mmol/L? Is there any recommendation for post-dialysis serum concentration?
In nephrologists' clinical experience, the overactivation of the complement alternative pathway (AP) is acquiring more and more importance in kidney failure etiopathogenesis. Indeed AP is involved in membranoproliferative glomerulonephritis, in atypical hemolytic uremic syndrome, in post-infectious glomerulonephritis, and now we are debating about a role of AP complement overactivation in ANCA associated vasculitis, in MGUS related nephrophaties.....Often patients with an AP dysregulation simulate Lupus without Lupus antibodies (SLE without SLE) and we observed some patients that overlaps with hypocomplementemic cutaneous vasculitis and/or cryoglobulinemic vasculitis
A 65 year old woman with CKD (urate nephropathy) with severe chronic asymptomatic hyponatremia (S-Na 121 mmol/L), elevation of creatinin kinase (7 ukat/L), polyuria (3600ml/day), polydipsia. No episodes of seizures, no clinical signs of dehydration, no medications affecting diuresis or natriuresis.
Serum Na 121, K 4, Cl 82, P 1.31, Ca 2.5, urea 9.2 mmol/L, OSM 254 mmol/kg, creatinine 97 umol/L, CK 7 ukat/L.
Urine Na 36, K 9, Cl 26 , P 3.7, Ca 0.21, urea 59, creatinine 1.28 mmol/L, OSM 147 mmol/kg.
Fractional excretion of Na 2.25%, OSM 4.4%, water 7.6%, urea 48.6%.
pH 7.41, pCO2 5.9 kPa, HCO3 28 mmol/L. Creatinine clearance 0.56 ml/s.
After 4 hours of fluid restriction diuresis was 400ml, increased urine osmolality from 147 to 265 mmol/L, increased urine sodium from 36 to 57 mmol/l, slightly decreased serum osmolality from 254 to 252 mmol/kg, serum sodium remained unchanged.
What is the diagnosis?
Is it water diuresis? Serum osmolality is higher than urinary, but fractional excretion of osmolal substances is high.
Could be primary polydipsia - urine osmolality increased after water restriction, so probably it is not diabetes insipidus, ADH should be present, at least partially.
Why did serum sodium not increase after fluid restriction? Could it be the combination of primary polydipsia and decreased tubular reabsorption of sodium (urate nephropathy)? Why is CK elevated without episodes of seizures?
Thank you for your opinions.
Why is the dexamethazone is not used widely as anti inflammatory agent compared to the prednizolone or methyleprednizolone inspite of being more potent than them and even not for short time use ( like the methylprednizolone use in the rapidly progressive glomerulonephritis for 5 days as pulse therapy)
It is very important to have a surveillance system for early diagnosis of HCV infection in dialysis centers and for control of it we should attend to some strategies, such as:
1. Less transfusion, more use of erytropoithin.
2. More education for the nurses in dialysis centers.
3. Treatment of HCV infected patients.
Do you agree with dedication of HCV infected from non-infected patients in dialysis centers?
I am interested in developing a trial model implementing intraperitoneal (IP) administration of heparin in GI cancer surgery (with special interest in cytoreductive surgery and hyperthermic intraperitoneal chemotherapy -HIPEC), combining intra-operative and post-operative administrations. I would appreciate if somebody can share his/her relevant experience regarding any aspects of IP use of heparin (subtypes, doses, complications, effect on peritoneal membrane, anti-cancerous/immuno-regulating properties, etc). Thank you in advance.
Renal stone is a prevalent disease with loud symptoms, and osteoporosis a prevalent and silent disease. I read about their relation and the role of IL6, but I would like to hear details about your clinical experience. As a GP or specialist, do you ask for a bone mineral density (BMD) for renal stone patients or at least for some of them? Or even think about the probability of low BMD in them? Do you have any experience of pathological fracture and patients with renal stone?
I recently used a serum creatinine assay kit from abcam (link below) and obtained some unexpected results. I was wondering if anyone here could share their experience with measurement of serum creatinine that could possibly shed light on what's going wrong:
Serum samples taken from 2010 to 2011 from elderly patients with prostate cancer were stored at -80 degrees Celsius, previously aliquoted, hence at the time of assay at most two or three freeze thaw cycles would've been performed.
This assay is based on conversion of creatinine to sarcosine, which is then oxidised and reacts with a probe to produce red colour measured with a spectrophotometer set at 570nm. The reaction is performed using a reaction mix containing all supplied enzymes and then again without creatininase in the reaction mix to account for background. The concentration is determined from the difference between the sample reading and its background.
I ended up with measurements of serum creatinine around 10pg/microlitre whereas the normal range is 45 to 110pg/microlitre. I tested serum samples from three subjects, and all of them had around 10pg/uL. If I don't subtract background, the serum creatinine concentration would calculate to be at the lower end of the normal range, however the absorbance reading of the background is high enough that it can't be ignored. The serum samples had varying amounts of haemolysis, but the background reading should account for this. If anything, haemolysis should overestimate the concentration, not underestimate it. The concentration of 10pg/uL appears to be way below the lower limit of the normal range.
I did not dilute the serum samples.
The standard curve was linear and covered 0 to 200pg/uL, with absorbances from 0.0052 (water + reaction mix in the well) to 1.778, which suggests I didn't dilute the standards incorrectly either (given that our spectrophotometer measures from 0.000 to 4.000).
So far I can only think of three explanations, the first that the serum samples were diluted (I have confirmed that this is not the case), secondly that the 2 or 3 freeze-thaw cycles have caused significant degradation of creatinine (unlikely), and thirdly that perhaps there's something in the serum that is inhibiting the enzymes (unlikely, given that this assay is optimised for serum samples). What could possibly explain these unexpected results, and how may I be able to fix this problem?
If anyone could help, it would be much appreciated.