S.PRADEEP KUMAR GOUD :THESIS AKI(2020-2022)
TOPIC:
AETIOLOGY AND OUTCOME IN ACUTE KIDNEY INJURY DUE TO MEDICAL DISORDERS IN KIMS NARKETPALLY
PROBLEM STATEMENT
Acute Kidney Injury (AKI) is a common clinical syndrome with a broad aetiological profile. It comprises about 5% of hospital admissions and 30% of admissions to intensive care units (ICU). It is associated with major morbidity and significant mortality due to the severity of the causative illness.
The true incidence of AKI is not easily discerned from published reports because of variation in methods of case ascertainment, definitions of AKI, and catchment populations1
Aetiology of Acute Kidney Injury varies from one geographic region of the world to another. While AKI secondary to diarrhoeal diseases, toxins, septic abortions, and other infections and environmental conditions are the common causes in the tropical countries, AKI following trauma due to high-speed traffic and industrial accidents, complex cardiovascular surgery, nephrotoxic drugs and chemicals, and cardiogenic shock are more prevalent in the industrialized world.1,2
In this perspective,I have endeavoured to study the various etiologies of Pre-renal, Renal and Post-renal AKI,their management and to analyse outcome of AKI pertaining to the aetiology,in our hospital (Kamineni Institute of medical sciences) during a specified period
AIM :
To study the aetiological profile and out come in Acute Kidney injury patients
OBJECTIVES :
1.To determine aetiological of prerenal, renal and post renal types of acute kidney injury.
2.To study the management of pre renal ,renal and post renal types of acute kidney injury.
3.To ascess the outcomes of acute kidney injury
MATERIALS AND METHODS :
PLACE OF STUDY : Department of General Medicine, Kamineni Institute of Medical Sciences, Narketpally.
STUDY PERIOD : October 2020-September 2022
STUDY DESIGN : Prospective Study, Observational study
SAMPLE SIZE : No.of cases to be studied = 50
INCLUSION CRITERIA :
Diagnostic criteria used in this study are a relevant history which could have precipitated Acute Kidney Injury symptoms like
1.Oliguria (urine output less than 400ml/day or less than 20ml / hour) anuria (less than 100ml in 24 hours)
2.Elevated renal parameters like urea (Normal value 15-45mg%), Creatinine (Normal: 0.6-1.2 mg%)
3.Non oliguric patients with elevated renal parameters.
4.Other symptoms those considered are oedma legs, facial puffiness, dyspnoea, vomiting and hiccup, if they fulfill the above criteria
EXCLUSION CRITERIA :
1)Patients with Pre existing chronic renal failure or chronic renal disease
2)Patients aged below 12years
METHOD OF DATA COLLECTION :
1) It is a prospective, observational study with 50 random cases of
renal failure satisfying my inclusion and exclusion criteria .
2) After taking informed consent a thorough evaluation was done
by a detailed history, physical examination,urinary analysis,
complete blood picture,renal function test,ultrasound abdomen,urinary
sodium,spot urine protien creatine ratio,fraction excretion of urine,liver
function test.
3) Few other investigations like blood and urine cultures whenever required
4)After admission patient will be evaluated for the etiology of renal
failure.Data will be collected on patient treatement (conservative
or hemodialysis),outcome during the hospital stay and follow up
after 3months of discharge
RESULTS :
TABLE:1 DISTRIBUTION OF CASES BASED ON AGE (n=50)
AGE IN YEARS | NO. OF PATIENTS | PERCENTAGE |
15-20 | 2 | 4% |
21-30 | 3 | 6% |
31-40 | 5 | 10% |
41-50 | 6 | 12% |
51-60 | 12 | 24% |
61-70 | 14 | 28% |
71-80 | 8 | 16% |
Out of 50 patients studied,majority were between the age group of 61-70(28%)
TABLE 2: DISTRIBUTION OF CASES BASED ON GENDER (n=50)
GENDER | NO OF PATIENTS(N) | PERCENTAGE |
MALE | 29 | 58% |
FEMALE | 21 | 42% |
TOTAL | 50 | 100% |
Out of 50 patients studied 29 are males(58%),21 are females(42%).
TABLE 3:DISTRIBUTION OF CASES BASED ON AETIOLOGY OF RENAL FAILURE
(n=50)
PRE-RENAL | Causes | No of cases(n=50) | |
Acute Gastro enteritis | 10(20%) | ||
Acute Pancreatitis | 2(4%) | ||
Heart Failure | 3(6%) | ||
Dengue | 2(4%) | ||
Liver Failure | 2(4%) | ||
DKA | 1(2%) | ||
Total | 20 | ||
RENAL | Sepsis | 19(38%) | |
Upper UTI | 3(6%) | ||
Connective Tissue Disease | 3(6%) | ||
Leptospirosis | 1(2%) | ||
Snake Bite | 1(2%) | ||
Multiple Myeloma | 1(2%) | ||
Total | 28 | ||
POST RENAL | Obstructive uropathy | 2(4%) |
TABLE 4: DISTRIBUTION OF CASES BASED ON TYPE OF ACUTE KIDNEY INJURY (n=50)
TYPE OF ACUTE KIDNEY INJURY | NO. OF PATIENTS | PERCENTAGE |
PRE RENAL | 20 | 40% |
INTRINSIC RENAL | 28 | 56% |
POST RENAL | 2 | 4% |
TOTAL | 50 | 100% |
Among 50 patients,28 patients presented with Renal AKI disease(56%),20 patients presented with
Pre-renal AKI disease(40%),2 patients presented with Post renal AKI disease(4%)
TABLE 5:DISTRIBUTION OF CASES BASED ON MANAGEMENT OF AKI (n=50)
TOTAL NO OF PATIENTS (N=50) | CONSERVATIVE MANAGEMENT | DIALYSIS THERAPY |
50 | 31 | 19 |
Out of 50 patients 31patients were conservatively treated(62%),19patients underwent Hemodialysis(38%)
TABLE 6:DISTRIBUTION OF CASES BASED ON MANAGEMENT IN TYPES OF ACUTE KIDNEY INJURY (n=50)
TYPES OF AKI | NO OF PATIENTS(n=50) | CONSERVATIVE | HEMODIALYSIS | ||
NO OF PATIENTS | PERCENTAGE | NO OF PATIENTS | PERCENTAGE | ||
PRE RENAL | 20 | 17 | 85% | 3 | 15% |
RENAL | 28 | 14 | 50% | 14 | 50% |
POST RENAL | 2 | --- | ---- | 2 | 100% |
All of post renal and 50% of renal type of acute kidney injury required dialysis.
TABLE 7: DISTRIBUTION OF CASES BASED ON MORTALITY (n=50)
NO OF PATIENTS STUDIED | NO.OF PATIENTS EXPIRED | MORTALITY RATE |
50 | 8 | 16% |
TABLE 8:DISTRIBUTION OF CASES BASED ON MORTALITY IN TYPES OF ACUTE KIDNEY INJURY (n=50)
AKI CAUSE | NO OF CASES (n) | SURVIVED | EXPIRED |
PRE-RENAL | 20 | 16 | 0 |
RENAL | 28 | 20 | 8 |
POST RENAL | 2 | 2 | 0 |
Mortality of 28% was seen in renal type of acute kidney injury
TABLE 9:DISTRIBUTION OF CASES WITH ACUTE KIDNEY INJURY PROGRESSED TO CHRONIC KIDNEY DISEASE (n=50)
AKI | NO OF CASES(n=50) | 3 Months follow up |
PRE RENAL | 20 | 0 |
RENAL | 28 | 3 |
POST RENAL | 2 | 0 |
TABLE 10:DISTRIBUTION OF CASES OF PRE RENAL AKI WITH RESPECT TO MORTALITY(n=20)
AKI | ETIOLOGY | NO OF CASES | SURVIVED | DEATH |
PRE RENAL | ACUTE GASTRO ENTERITIS | 10 | 10 | 0 |
ACUTE PANCREATITIS | 2 | 2 | 0 | |
HEART FAILURE | 3 | 3 | 0 | |
DENGUE | 2 | 2 | 0 | |
LIVER FAILURE | 2 | 2 | 0 | |
DIABETIC KETO ACIDOSIS | 1 | 1 | 0 | |
TOTAL | 20 | 20 | 0 |
TABLE 11:DISTRIBUTION OF CASES WITH RENAL AKI WITH RESPECT TO MORTALITY(n=28)
AKI | ETIOLOGY | NO OF CASES(n=28) | SURVIVED | DEATH |
RENAL | SEPSIS | 19 | 12 | 7 |
UROSEPSIS | 3 | 3 | 0 | |
CONNECTIVE TISSUE DISORDER | 3 | 3 | 0 | |
LEPTOSPIROSIS | 1 | 1 | 0 | |
SNAKE BITE | 1 | 1 | 0 | |
MULTIPLE MYELOMA | 1 | 0 | 1 | |
TOTAL | 28 | 20 | 8 |
TABLE 12:DISTRIBUTION OF CASES WITH POST RENAL AKI WITH RESPECT TO MORTALITY(n=2)
AKI | ETIOLOGY | NO OF CASES | SURVIVED | DEATH |
POST RENAL | OBSTRUCTIVE UROPATHY | 2 | 2 | 0 |
TABLE 13:DISTRIBUTION OF CASES WITH RENAL AKI WITH RESPECT TO CAUSE OF MORTALITY(n=8)
AKI | CAUSE OF MORTALITY | NO OF CASES(n=8) |
RENAL | MODS WITH SHOCK | 5 |
CARDIOGENIC SHOCK | 1 | |
SUDDEN CARDIAC ARREST | 2 |
DISCUSSION
This is a prospective observational study conducted in Kamineni Institute of Medical Sciences Narketpally in General Medicine Department from october 2020 to october 2022 in 50 renal failure patients
AGE COMPARED WITH OTHER STUDIES
In the present study, out of 50 patients 34 (68%) of them were of the age 60 years and above ,consistent with study done by Liano et al(17) in Madrid , showed a mean age of 64years in patients with acute kidney injury,Meran et al(18) in United Kingdom ,showed a mean age of 73years in patients with acute kidney injury.
GENDER COMPARED WITH OTHER STUDIES
In this study of 50 patients,29 patients (58% )are males and 21patients (42%) are females similar to study done by Sanjay Vikranth et.al in Shimla India with a male predominance of 62% and Fan Yang et.al in China with a male predominance of 57%.
TABLE 14:COMPARISION OF ETIOLOGY OF RENALFAILURE WITH OTHER STUDIES
STUDY | STUDY PERIOD | PLACE OF STUDY | NO OF PATIENTS(n) | PRE-RENAL AKI | RENAL AKI | POST RENAL AKI |
THANDIWE A.L.DLAMINIet al29 | 2012-2013 | South Africa | 366 | 128 (34.7%) | 223(60.7%) | 17(4.6%) |
FAN YANG et al 1 | 2013 | China | 271 | 99(36.5 %) | 126(46.5%) | 46(17%) |
AIDA HAMZIC MEHMED BASIC et al 2 | 2015 | United kingdom | 84 | 38(45.2%) | 36(42.8%) | 10(12%) |
SU HOOI TEO et al 11 | 2016-2017 | singapore | 404 | 112(27.7%) | 283(70.1%) | 9(2.2%) |
SANJAY VIKRANTH et al28 | 2018 | Shimla | 309 | 125(40.5%) | 164(53%) | 20(6.5%) |
Present Study | 2020-2022 | Narketpally | 50 | 20(40%) | 28(56%) | 2(4%) |
In our study group prerenal and intrinsic type were detected in
40% and 56% of AKI patients, respectively, while post renal type
of AKI was recognized only in 4% of patients. The prevalence of
pre-renal and intrinsic causes was similar to the occurrence of
renal causes in the study of FAN YANG et al(1),AIDA HAMZIC
MEHMED BASIC et al (2),SANJAY VIKRANTH(28),THANDIWE
A.L.DLAMINIet al(29),while post renal AKI was less frequent.In
study done by SU HOOI TEO et al(11) Pre renal,renal was 27.7%
and 70.1% respectively.
TABLE 15:COMPARISION OF INDIVIDUAL ETIOLOGIES OF RENALFAILURE WITH OTHER STUDIES
STUDY | STUDY PERIOD | PLACE OF STUDY | NO OF PATIENTS(n) | PRE-RENAL AKI | RENAL AKI | POST RENAL AKI |
THANDIWE A.L.DLAMINIet al29 | 2012-2013 | South Africa | 366 | Acute Gastroenteritis-12.8% Acute pancreatitis-4.4% | sepsis-60.7% Multiple Myeloma-0.82% Urosepsis-7.4% | Obstructive uropathy-4.6% |
FAN YANG et al 1 | 2013 | China | 271 | Acute Gastroenteritis-10.7% Heart failure- 11.8% DKA-1.5% | sepsis-30.6% Urosepsis-8.5% | Obstructive uropathy-17% |
AIDA HAMZIC MEHMED BASIC et al 2 | 2015 | United kingdom | 84 | Acute Gastroenteritis13% Heart failure-15% | Sepsis-12% Multiple Myeloma-1% Leptospirosis-1% | Obstructive uropathy-6% |
SANJAY VIKRANTH et al28 | 2018 | Shimla | 309 | Acute Gastroenteritis-6.5% Acute pancreatitis-2.9% Heart failure-7.4%% | sepsis-52% Leptospirosis-1% | Obstructive uropathy-6.5% |
Present study | 2020-2022 | Narketpally | 50 | Acute Gastroenteritis-20% Acute pancreatitis-4% Heart failure-6% DKA-2% | Sepsis-38% Multiple Myeloma-1% Leptospirosis-1% Urosepsis-6% | Obstructive uropathy-4% |
In the present study individual etiologies of
1)Pre renal causes-
Acute Gastroenteritis(20%),Heart Failure(6%),Acute
pancreatitis(4%),DKA(2%)
2)Renal causes-
Sepsis(38%),Urosepsis(6%),Multiple myeloma(1%),Leptospirosis(1%)
3)Post renal causes-
Obstructive uropathy(4%)
were similar to occurence in the study of AIDA HAMZIC
MEHMED BASIC et al (2) ,THANDIWE A.L.DLAMINIet al29,FAN YANG et al 1
SANJAY VIKRANTH et al28
TABLE 16:COMPARISION OF TREATMENT OF RENALFAILURE WITH OTHER STUDIES
STUDY | STUDY PERIOD | PLACE OF STUDY | NO OF PATIENTS | NO OF [PATIRNTS UNDERWENT DIALYSIS | NO OF PATIENTS CONSERVATIVELY MANAGED |
THANDIWE A.L.DLAMINI et al29 | 2012-2013 | South Africa | 366 | 204(55.7%) | 162(44.2%) |
AIDA-HAMZIC-MEHMEDBASIC et al2 | 2015 | United kingdom | 84 | 18(21%) | 66(79%) |
SU HOOI TEO et al 11 | 2016-2017 | singapore | 404 | 107(27%) | 297(73%) |
SANJAY VIKRANTH et al28 | 2018 | Shimla | 309 | 72(23.3%) | 237(76.6%) |
TEUWAFEU DENIS GEORGES et al 5 | 2021 | Cameroon | 349 | 168(48%) | 181(52%) |
Present study | 2020-2022 | Narketpally | 50 | 19(38%) | 31(62%) |
In present study hemodialysis was carried out in 38% of our AKI
patients, which is consistent with the proportion of AKI patients
who received hemodialysis (48%) in the study of TEUWAFEU
DENIS GEORGES et al (5).Dialysis requirement in different
studies ranged from 12% to 71% (1,2,6,7,11,28,29).
TABLE 17:COMPARISION OF MORTALITY IN RENALFAILURE WITH OTHER STUDIES
STUDY | STUDY PERIOD | PLACE OF STUDY | NO OF PATIENTS | MORTALITY |
THANDIWE A.L.DLAMINI et al29 | 2012-2013 | South Africa | 366 | 114(31.2%) |
FAN YANG et al1 | 2013 | China | 271 | 53(19.6%) |
AIDA-HAMZIC-MEHMEDBASIC et al2 | 2015 | United kingdom | 84 | 9(10.7%) |
SU HOOI TEO et al 11 | 2016-2017 | singapore | 404 | 82(20.3%) |
SANJAY VIKRANTH et al28 | 2018 | Shimla | 309 | 27(8.7%) |
ABDUL KAREEM et al27 | 2018-2020 | Pakistan | 267 | 11(4.2%) |
Present Study | 2020-2022 | Narketpally | 50 | 8(16%) |
In the present study there is 16% mortality,were as in the
studies done by FAN YANG et al1,SU HOOI TEO et al11
THANDIWE A.L.DLAMINI et al29,AIDA-HAMZIC-MEHMEDBASIC
et al2 ,SANJAY VIKRANTH et al28 ,ABDUL KAREEM et al27
mortality was
' 19.6%,20.3%,31.2%,10.7%,8.7%,4.2%respectively.
TABLE 18:COMPARISION BETWEEN OTHER STUDIES SHOWING SESPSIS AS PREDOMINANT CAUSE OF RENAK AKI
STUDY | STUDY PERIOD | PLACE OF STUDY | NO OF PATIENTS(n) | RENAL AKI CAUSED BY SEPSIS |
THANDIWE A.L.DLAMINIet al29 | 2012-2013 | South Africa | 366 | 60.7% |
FAN YANG et al 1 | 2013 | China | 271 | 30.6% |
SANJAY VIKRANTH et al28 | 2018 | Shimla | 309 | 53.1% |
Present Study | 2020-2022 | Narketpally | 50 | 38% |
In the present study sepsis as the major etiology of renal AKI
seen in 38% of the total cases which is consistent with other
studies ,
60.7%THANDIWE A.L.DLAMINI.etal29,
53.1%SANJAY VIKRANTH et al28,
30.6%FAN YANG et al1.
SUMMARY
1)In my study of 50 patients,29 patients (58% )are males and 21 patients (42%) are females
2)In the present study majority of patients were over 60 years of age and the most of them were males(58%)
3)Age older than 65 is not only a risk factor for immediate recovery from AKI and progression to advanced stage CKD, but the long-term survival of patients with AKI worsens with increasing age, even in non-dialysis requiring AKI [19–21].
4)In our study group prerenal and intrinsic type were detected in 40% and 56% of AKI patients respectively, while post renal type of AKI was recognized only in 4% of patients
5)In the present study individual etiologies of
1)Pre renal causes-
Acute Gastroenteritis(20%),Heart Failure(6%),Liver
failure(2%),Acute pancreatitis(2%),Dengue(2%),Diabetic keto
acidosis(1%)
2)Renal causes-
Sepsis(38%),Upper UTI(6%),Connective tissue
disorder(6%),Multiple myeloma(1%),Leptospirosis(1%),snake bite(1%)
3)Post renal causes-
Obstructive uropathy(4%)
6)The main etiological factors of AKI in our present study were Sepsis(38%),Acute Gastroenteritis(20%),Heart Failure and Connective tissue disorder(6%),other etiologies less than 5%.In
the PICARD study and BEST Kidney study (3,4) Sepsis and Acute Gastroenteritis were among four most common AKI causes which is consistent to our findings
7)In present study hemodialysis was carried out in 38% of our AKI patients
8)An episode of dialysis-requiring AKI was a strong independent risk factor for long-term risk of progressive CKD and mortality(22)
9)Recognizing that AKI survivors are at high risk of progressiveCKD spurred the Kidney Disease Improving Global Outcomes (KDIGO) AKI guidelines to recommend that the kidney function should be evaluated 3 months after an AKI episode to establish the presence and extent of CKD (8), which was done
in our study.
10)Of the cases followed up 3 AKI cases progressed to CKD
11)In the previously published studies (9,10) sepsis was found to be associated with mortality which is in accordance with our findings
12)Sepsis is the most common cause of AKI in ICU (7). Recent evidence suggests that AKI in patients with sepsis may have different pathophysiology including hyperemia, vasodilatation and acute tubular apoptosis instead of ischemia,vasoconstriction or acute tubular necrosis (11).
13) The mortality of sepsis induced AKI is more than 70% (11). Our findings suggest that septic cause of AKI is more common in non-survivors compared to survivors, as well as that sepsis is risk factor for death in AKI patients.
14)Multiple AKI biomarkers that are measured in the urine or plasma of patients with AKI have been discovered, including the neutrophil gelatinase-associated lipocalin (NGAL), kidney injury
molecule 1 (KIM-1), liver-type fatty acid-binding protein (L-FABP),interleukin 18 (IL-18), calprotectin, urine angiotensinogen (AGT),urine microRNAs and the recently FDA-approved insulin-like growth factor-binding protein 7x tissue inhibitor of metalloproteinase 2 in the USA(23)
15)Biomarkers for AKI diagnosis are not currently being used routinely in our local clinical practice, hence our study did not include any novel biomarkers for AKI diagnosis. In our future research, we hope to leverage the relationship of biomarkers in diagnosing AKI and predicting short and
longterm outcomes of acute kidney injury in different patient care settings, given the heterogeneity of this condition
CONCLUSION
1)From the present study it is concluded that sepsis is the most common cause of renal AKI in critically ill patients.Sepsis with multi organ dysfunction is the chief reason of high mortality in my study.It is highly essential to prevent the emergence of multi organ failure in any case of sepsis.
2)Our patients were managed consevatively and with hemodialysis whenever indicated
.
3)From my study it can be concluded that Multi organ failure in the setting of sepsis should be treated aggressively to decrease the high mortality.
REFERENCES
1)Yang F, Zhang L, Wu H, Zou H, Du Y. Clinical analysis of cause, treatment and prognosis in acute kidney injury patients. PLoS One. 2014 Feb 21;9(2):e85214. doi: 10.1371/journal.pone.0085214. PMID: 24586237; PMCID: PMC3931618.
2)Hamzic-Mehmedbasic A, Rebic D, Balavac M, Muslimovic A, Dzemidzic J. Clinical analysis of etiology, risk factors and outcome in patients with acute kidney injury. Mater Sociomed. 2015 Apr;27(2):70-4. doi: 10.5455/msm.2015.27.71-74. Epub 2015 Apr 5. PMID: 26005378; PMCID: PMC4404958.
3)Mehta RL, Pascual MT, Soroko S, Savage BR, Himmelfarb J, Ikizler TA, Paganini EP, Chertow GM. Program to Improve Care in Acute Renal Disease. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. 2004; 66(4): 1613-1621.
4)Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morg-era S, Schetz M, Tan I, Bouman C, Macedo E, Gibney N, Tolwani A, Ronco C. Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005; 294(7): 813-818.
5) Georges TD, Marie-Patrice H, Ingrid TS, Mbua RG, Hermine FM, Gloria A. Causes and outcome of acute kidney injury amongst adults patients in two hospitals of different category in Cameroon; a 5 year retrospective comparative study. BMC Nephrol. 2022 Nov 14;23(1):364. doi: 10.1186/s12882-022-02992-4. PMID: 36376867; PMCID: PMC9661768.
6) Piccinni P, Cruz DN, Gramaticopolo S, Garzotto F, Dal Santo M, Aneloni G, Rocco M, Alessandri E, Giunta F, Michetti V, Iannuzzi M,Belluomo Anello C, Brienza N, Carlini M, Pelaia P, Gabbanelli V, Ronco C; NEFROINT Investigators. Prospec- tive multicenter study on epidemiology of acute kidney injury in the ICU: a critical care nephrology Italian collaborative effort (NEFROINT). Minerva Anestesiol. 2011; 77(11): 1072-1083.
7) Bagshaw SM, Uchino S, Bellomo R, Morimatsu H, Morgera S, Schetz M, Tan I, Bouman C, Macedo E, Gibney N, Tolwani A, Oudemans-van Straaten HM, Ronco C,Kellum JA. For the Be- ginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Septic acute kidney injury in critically ill patients: clinical characteristics and outcomes. Clin J Am Soc Nephrol. 2007; 2(3): 431-439.
8) Ad-hoc working group of ERBP, Fliser D, Laville M, et al. A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant. 2012; 27(12): 4263-4272.
9)Daher EF, Marques CN, Lima RS, Silva Júnior GB, Barbosa AS, Barbosa ES, Mota RM, Leite da SilvaS, Araújo SM, Libório AB. Acute kidney injury in an infectious disease intensive care
unit-an assessment of prognostic factors. Swiss Med Wkly. 2008; 138(9-10): 128-133.
10)Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S, Schetz M, Tan I, Bouman C, Macedo E, Gibney N, Tolwani A, Ronco C. Beginning and Ending Supportive Th erapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005; 294(7): 813-818.
11)Wan L, Bagshaw SM, Langenberg C, Saotome T, May C, Bel_x0002_lomo R. Pathophysiology of septic acute kidney injury: What do we really know? Crit Care Med. 2008; 36(4 Suppl): S198-S203
12)Teo, S.H., Lee, KG., Koniman, R. et al. A prospective study of clinical characteristics and outcomes of acute kidney injury in a tertiary care Centre. BMC Nephrol 20, 282 (2019).
13)Waikhom R, Sircar D, Patil K, Bennikal M, Gupta SD, Pandey R (2012) Long-term renal outcome of snake bite and acute kidney injury: a single-center experience. Ren Fail 34:271–274
14)Herath HM, Wazil AW, Abeysekara DT, Jeewani ND, Weerakoon KG, Ratnatunga NV, Bandara EH, Kularatne SA. Chronic kidney disease in snake envenomed patients with acute kidney injury in Sri Lanka: a descriptive study. Postgrad Med J. 2012 Mar;88(1037):138-42. doi: 10.1136/postgradmedj-2011-130225. Epub 2012 Jan 25. PMID: 22282736.
15) Jayawardana S, Arambepola C, Chang T, Gnanathasan A (2018) Long-term health complications following snake envenoming. J Multidiscip Healthc 11:279–285
16) Dineshkumar T, Dhanapriya J, Murugananth S, Surendar D, Sakhthirajan R, Rajasekar D, Balasubramaniyan T, Gopalakrishnan N (2018) Snake envenomation-induced acute in- terstitial nephritis. J Integr Nephrol Androl 5:14–17
17) Liaño F, Pascual J. Epidemiology of acute renal failure: a prospective,multicenter, community-based study. Madrid Acute Renal Failure study group. Kidney Int. 1996;50(3):811–8
18)Meran S, Wonnacott A, Amphlett B, Phillips A. How good are we at managing acute kidney injury in hospital? Clin Kidney J. 2014;7(2):144–50
19)31. Anderson S, Eldadah B, Halter JB, Hazzard WR, Himmelfarb J, Horne FM, et al.Acute kidney injury in older adults. J Am Soc Nephrol. 2011;22(1):28–38.
20)Schmitt R, Coca S, Kanbay M, Tinetti ME, Cantley LG, Parikh CR. Recovery of kidney function after acute kidney injury in the elderly: a systematic review and meta-analysis. Am J Kidney Dis. 2008;52(2):262–71.
21)Cerda J, Lameire N, Eggers P, Pannu N, Uchino S, Wang H, et al. Epidemiology of Acute kidney injury. Clin J Am Soc Nephrol. 2008;3(3):881–6.
22) Lo LJ, Go AS, Chertow GM, McCulloch CE, Fan D, Ordoñez JD, et al. Dialysis_x0002_requiring acute renal failure increases the risk of progressive chronic kidney disease. Kidney Int. 2009;76(8):893–9.
23)Kashani K, Cheungpasitporn W, Ronco C. Biomarkers of acute kidney injury:the pathway from discovery to clinical adoption. Clin Chem Lab Med. 2017; 55(8):1074–89.
24) Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. Am JKidney Dis 39: 930–936, 2002
25) Kathaleen D, Gleen M, Harrisons principles of Internal medicine 17th edition pages 1753,1759-1760
26)Textor SC : renal failure related ACEI . semin nephrol 17; 67-76, 1997
27) Zarkoon, Abdul & Habib, Ullah & Rind, Moin & Khan, Aijaz & Ahmed, Nasir & Jakrani, Muhammad & Hussain, Hamid & Ali, Ul & Haq, Abdul & Mandokhail, Atta & Ullah, Faiza & Khalil, Abdul & Hameed, Ghulam & Kalwar, Hamid, AKI Etiology & Outcomes Etiology and Outcomes of Acute Kidney Injury in Patients Admitted to a Single Tertiary Care Hospital: Balochistan Institute of Nephrology-Urology Quetta,Pak J Kidney Dis 2020;4(4):319-323
28)Vikrant S, Gupta D, Singh M. Epidemiology and outcome of acute kidney injury from a tertiary care hospital in India. Saudi J Kidney Dis Transpl 2018;29:956-66
29)Dlamini TAL, Heering PJ, Chivese T, Rayner B (2017) A prospective study of the demographics, management and outcome of patients with acute kidney injury in Cape Town, South Africa.PLoS ONE 12(6): e0177460
PROFORMA
CLINICAL STUDY OF ACUTE RENAL FAILURE
Name:
Age / Sex:
Ward
IP NO
AETIOLOGY:
HISTORY:
Past history
III CLINICAL EXAMINATION:
1. Pulse Rate
Volume
2. Blood Pressure
3. Respiratory Rate
4. Temperature:
5. Pallor
6. Jaundice
7. Hydration
8. Others
Investigations
A)Blood
Urea(mg/dl)
Creatinine(mg/dl)
Sugar(Random)(mg/dl)
Serum electrolytes(meq/L)
Total Count(Per cu.mm)
Differential count(%)
Hemoglobin(gm/dl)
B)URINALYSIS
Albumin
Sugar
Deposits
Urine Sodium(meq/L)
Spot urine protien creatinine ratio
C)Ultrasonogram-Abdomen
3)Diagnosis
4) Treatment
Conservative
Hemodialysis
5)Outcome
Recovered
Succumbed
6)Follow up after 3months
PATIENT INFORMATION SHEET
English:
https://drive.google.com/file/d/12LLDgFBVfnTxDdNv5K715uSyLYPUEgrY/view?usp=drivesdk
Telugu:
https://drive.google.com/file/d/13Df9wCu9zhjECpPxcHEULSAphv6-tDHl/view?usp=drivesdk
Template of this "patient information sheet" is borrowed from this website:
https://www.ncbi.nlm.nih.gov/books/NBK261334/
And modified accordingly to my thesis topic.
Link to master chart
LEARNING POINTS :-
One of the main reason to select the topic of AKI is,My dad who is diabetic(since 25years) had urosepsis(secondary to ascending pyelonephritis) in 2019 landed in AKI(sr creat-7.7mg/dl),with conservative treatment his creatinine became normal(1.1mg/dl with in one month).Even though he recovered i am still having fear that wether he will land in CKD.This is the seed that had planted in my mind before starting my pg study
I have taken up my thesis from 2020 to 2022 to see what are the different etiological factors of AKI,their treatment(conservative/dialysis),their outcomes & progression to CKD.
What i have learned from my thesis is
1)Following up cases is very important rather than single point of care in hospital .
2)In the diagnosis part of AKI,rather than relaying on the laboratory parameters(like Urine electrolytes,Fractional excretion of urine,Renal failure index),history and initial treatment(i.e first 24hr’s) is more important in classification of disease(as pre-renal/renal/post renal)
3)Calibration of Spot urine electrolytes in the book is different from working laboratory (i have checked different labs-kims nkp lab,KHL Lab,Thyrocare lab-All the labs are having same reference values) UNCERTAINTY STILL PERSIST
4)My hunt for what kind of AKI etiologies land in to CKD have been fulfilled .After 2years with the thesis cases i realised most(50%) of the renal AKI patients required dialysis(Majority of sepsis related Renal AKI patients) & 6% of them landed in CKD.So etiology of AKI plays a very important role in it’s progression to CKD
Contribution to world from my thesis :-
More research should be done on biochemical parameters to have uniform reference values to add more accurate classification & diagnosis of AKI
Links to patients blogs :
Comments
Post a Comment