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Fulltext Acute Deterioration of Kidney Function after Total Hip Arthroplasty

Takeshita S, Sonohata M, Kitajima M, Kawano S, Eto S, Mawatari M

Malays Orthop J, 2020 Jul;14(2):111-119.
PMID: 32983385 DOI: 10.5704/MOJ.2007.020

Introduction: Post-operative acute kidney injury is a serious complication and identifying modifiable factors could assist in peri-operative management. This study aimed to identify the pre-operative and intra-operative factors associated with the incidence of post-operative acute kidney injury and acute deterioration of kidney function after total hip arthroplasty.Materials and methods: This single-center, retrospective, observational study included 203 patients who underwent unilateral primary total hip arthroplasty. Acute kidney injury was determined using biochemical markers according to the risk, injury, failure, loss of kidney function, and end-stage kidney disease (RIFLE) criteria. Acute deterioration of kidney function was defined as the reduction of estimated glomerular filtration rate by ≥10ml/min/1.73m2.
Results: Prior to total hip arthroplasty, 20% of all patients met the chronic renal dysfunction criterion of glomerular filtration rates <60ml/min/1.73m2 (glomerular filtration rate categories G3a-G5). Incidence rates of acute kidney injury and acute deterioration of kidney function after total hip arthroplasty were 0.49% and 6.9%, respectively. Multivariate regression analysis showed that diabetes mellitus and use of nonsteroidal anti-inflammatory drugs before total hip arthroplasty were significant risk factors for acute deterioration of kidney function. Advanced age, preoperative renal dysfunction, antihypertensive, diuretics, or statin use, operation time, total blood loss, type of anesthetic, and body mass index were not significant risk factors.
Conclusion: Diabetes mellitus and use of nonsteroidal anti-inflammatory drugs were controllable risks, and multidisciplinary approaches are a reasonable means of minimising peri-operative acute kidney injury or acute deterioration of kidney function.

Matched MeSH terms: Acute Kidney Injury
Acute kidney injury: epidemiology and course in critically ill children

Tai CW, Gibbons K, Schibler A, Schlapbach LJ, Raman S

J Nephrol, 2021 Jun 02.
PMID: 34076880 DOI: 10.1007/s40620-021-01071-5

BACKGROUND: Acute kidney injury (AKI) is a major cause of morbidity and mortality in critically ill children. The aim of this paper was to describe the prevalence and course of AKI in critically ill children and to compare different AKI classification criteria.
METHODS: We conducted a retrospective observational study in our multi-disciplinary Pediatric Intensive Care Unit (ICU) from January 2015 to December 2018. All patients from birth to 16 years of age who were admitted to the pediatric ICU were included. The Kidney Disease Improving Global Outcomes (KDIGO) definition was considered as the reference standard. We compared the incidence data assessed by KDIGO, pediatric risk, injury, failure, loss of kidney function and end- stage renal disease (pRIFLE) and pediatric reference change value optimised for AKI (pROCK).
RESULTS: Out of 7505 patients, 9.2% developed AKI by KDIGO criteria. The majority (59.8%) presented with stage 1 AKI. Recovery from AKI was observed in 70.4% of patients within 7 days from diagnosis. Both pRIFLE and pROCK were less sensitive compared to KDIGO criteria for the classification of AKI. Patients who met all three-KDIGO, pRIFLE and pROCK criteria had a high mortality rate (35.0%).
CONCLUSION: Close to one in ten patients admitted to the pediatric ICU met AKI criteria according to KDIGO. In about 30% of patients, AKI persisted beyond 7 days. Follow-up of patients with persistent kidney function reduction at hospital discharge is needed to reveal the long-term morbidity due to AKI in the pediatric ICU.

Matched MeSH terms: Acute Kidney Injury
Fulltext Idiopathic hypereosinophilic syndrome with unusual presentation: two case reports and review of literature

Suria, A.A., Hafizah, H., Nurasyikin, Y., Azlin, I., Yousuf, R., Azma, R Z., et al.

Medicine & Health, 2018;13(2):208-216.
MyJurnal

Idiopathic hypereosinophilic syndrome (HES) is an uncommon disorder which usually presents with prolonged and significant primary eosinophilia with end-organ dysfunction. Damaging proteins released by the eosinophilic granules are responsible for the tissues and organ system damage. Here we report two cases of idiopathic HES. Both the patients were young lady presented with high grade fever and concomitant symptoms. Laboratory findings showed leucocytosis with predominant neutrophilia and marked eosinophilia. A diagnosis of idiopathic HES was made after excluding secondary causes of eosinophilia. However, the first patient was complicated with multiple venous thrombosis and intravenous heparin was started which was later changed to subcutaneous low molecular weight heparin (LMWH). The patient developed pleural effusion and consolidation. Intravenous Tazoscin, tablet Prednisolone and tablet Hydroxyurea was started and the patient responded well. Despite treatment, two weeks later, suddenly the patient collapsed and unfortunately succumbed. On the other hand, the second patient was complicated with fever, thrombocytopenia, haemolytic anaemia, acute renal failure and neurological deficit which were part and parcel of thrombotic thrombocytopenic purpura (TTP). Plasma exchange was commenced and patient’s condition had slowly improved. Nevertheless, the hypoxia which she sustained during the multiple episodes of fits had resulted in permanent brain injury and thus requiring a tracheostomy for prolonged ventilatory support. Currently, there is no cure for HES. The main aim of treatment is to minimise the tissue damage caused by the hypereosinophilia. Early diagnosis and intervention are therefore crucial in preventing the spread of the disease and the end-organ damage.

Matched MeSH terms: Acute Kidney Injury
An unusual cause of acute abdomen and acute renal failure: Djenkolism

Sumitro K, Yong CS, Tan LT, Choo S, Lim CY, Shariman H, et al.

Malays Fam Physician, 2020;15(2):50-52.
PMID: 32843946

The djenkol bean (Archidendron pauciflorum) is a native delicacy in Southeast Asia, though consumption can sometimes lead to djenkolism. Clinical features of djenkolism include acute abdominal pain, hematuria, urinary retention, and acute kidney injury (AKI). The pain can be severe, which often leads to a misdiagnosis of acute abdomen. In this paper, we report the case of an Indonesian migrant with djenkolism. Due to the short history and severity of the abdominal pain, medical professionals suspected acute abdomen and proceeded with a negative exploratory laparotomy. However, djenkolism was suspected once relatives informed the professionals that the patient had consumed djenkol beans hours earlier. The patient recovered through aggressive hydration and urine alkalinization with bicarbonate infusion. We highlight the importance of being aware of this rare cause of AKI, especially in Southeast Asia, in order to provide early diagnoses and prompt treatments.

Matched MeSH terms: Acute Kidney Injury
Fulltext Bilateral stones and renal failure

Suleiman AB, Awang H, Proehoeman F

Med J Malaysia, 1981 Mar;36(1):14-6.
PMID: 7321931

The clinical presentation of patients with bilateral stones is discussed. The majority of patients presenting to the Nephrology Unit were in renal failure. Aggressive medical treatment allowed
diagnostic procedures and definitive surgery to be performed in uraemic patients. Most patients presenting in uraemia benefitted from treatment.
Study Site: Urology Unit, General Hospital, Kuala Lumpur, Malaysia

Matched MeSH terms: Acute Kidney Injury/etiology*; Acute Kidney Injury/therapy
Clinical review of acute renal failure: a 5-year experience at Kuala Lumpur

Suleiman AB

Ann Acad Med Singap, 1982 Jan;11(1):32-5.
PMID: 7073225

Over a five year period, 184 patients were treated for acute renal failure. Uraemia was usually treated by peritoneal dialysis, and haemodialysis was reserved for post surgical and hypercatabolic patients. The overall mortality was 33.2% and was highest among surgical patients. These results were similar to previous reports. Peritoneal dialysis was usually effective in controlling uraemia. Uncontrolled sepsis remains a major problem, and septicaemia and gastrointestinal bleeding were adverse factors affecting the outcome. The combination of septicaemia and gastrointestinal bleeding commonly led to a fatal outcome.

Matched MeSH terms: Acute Kidney Injury/etiology; Acute Kidney Injury/mortality; Acute Kidney Injury/therapy*
Fulltext Acute renal failure and hepatitis: a rare manifestation of typhoid Fever - a case report

Sulaiman W, Gunavathy M, Othman M

Malays J Med Sci, 2007 Jan;14(1):65-6.
PMID: 22593655 MyJurnal

Hepatitis complicating typhoid fever has been previously reported widely. Occurrence of acute renal failure and hepatitis together is exremenly rare. A case report of complicated acute renal failure and hepatitis in a tyhoid patient is reported and discussed.

Matched MeSH terms: Acute Kidney Injury
Experiences with dialysis at the General Hospital, Kuala Lumpur

Sreenevasan G

Br J Urol, 1970 Dec;42(6):741.
PMID: 5497398
Matched MeSH terms: Acute Kidney Injury/therapy*
Fulltext Adult pyloric stenosis masquerading as acute renal failure

Siow SL, Wong CM, Sohail M

Med J Malaysia, 2009 Jun;64(2):168-9.
PMID: 20058581 MyJurnal

Gastric outlet obstruction and in particular, pyloric stenosis, is relatively common in developing countries. Acute clinical presentation is often the manifestation of biochemical and electrolyte changes. The presence of metabolic alkalosis in combination with acute renal failure should alarm us to the possibility of adult pyloric stenosis. We report a case of adult pyloric stenosis that presented as acute renal failure and discuss its pathophysiology.

Matched MeSH terms: Acute Kidney Injury/etiology*
Renal diseases in pregnancy: a clinical review and appraisal

Sinnathuray TA

Med J Malaya, 1971 Jun;25(4):253-6.
PMID: 4261295
Matched MeSH terms: Acute Kidney Injury/complications
Djenkol bean poisoning (djenkolism): an unusual cause of acute renal failure

Segasothy M, Swaminathan M, Kong NC, Bennett WM

Am J Kidney Dis, 1995 Jan;25(1):63-6.
PMID: 7810535

This report describes a patient with acute renal failure that resulted from the ingestion of djenkol beans. Features of acute djenkolism include nausea, vomiting, bilateral loin pain, gross hematuria, and oliguria. The blood urea level was 16.2 mmol/L and the serum creatinine was 460 mumol/L. Phase contrast microscopy of the urinary sediment indicated that the hematuria was nonglomerular. Ultrasound of the kidneys showed slightly enlarged kidneys with no features of obstruction. Renal biopsy showed acute tubular necrosis similar to the single animal study reported in the literature. With conservative therapy, which included rehydration with normal saline and alkalinization of the urine with sodium bicarbonate, the acute renal failure resolved. Based on its chemistry, djenkol bean-associated acute renal failure may be analogous to acute uric acid nephropathy.

Matched MeSH terms: Acute Kidney Injury/blood; Acute Kidney Injury/etiology*; Acute Kidney Injury/pathology
Fulltext Acute renal failure in falciparum malaria

Segasothy M, Swaminathan M, Kong NC

Med J Malaysia, 1994 Dec;49(4):412-5.
PMID: 7674979

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.

Matched MeSH terms: Acute Kidney Injury/etiology*
Acute renal failure in 2K2C Goldblatt hypertensive rats during antihypertensive therapy: comparison of an angiotensin AT1 receptor antagonist and clonidine analogues

Sattar MA, Yusof AP, Gan EK, Sam TW, Johns EJ

J Auton Pharmacol, 2001 5 15;20(5-6):297-304.
PMID: 11350495

1. This study compared the effect of a non-peptide angiotensin II receptor antagonist and a series of clonidine analogues on blood pressure and renal function in a two-kidney two-clip Goldblatt rat model of hypertension subjected to 2 weeks of dietary sodium deprivation. 2. Animals received either vehicle, the angiotensin II antagonist, ZD7155 or structural analogues derived from clonidine (AL-11, AL-12 and CN-10) at 10 mg kg-1 day-1 for 4 days. 3. All groups of rats had systolic blood pressure in the hypertensive range (160-180 mmHg). ZD7155 caused a 33-mmHg fall in blood pressure (P < 0.05) and raised plasma urea and creatinine four- to six-fold. 4. AL-12 decreased blood pressure by 30 mmHg (P < 0.05), but had no effect on water intake, urine flow or plasma urea and creatinine. AL-11 and CN-10 had minimal effects on blood pressure and water intake and while CN-10 decreased urine flow on the third treatment day, AL-11 markedly reduced urine flow by some 70%. 5. These data show that in this sodium deficient renovascular model of hypertension, blockade of angiotensin II receptors normalizes blood pressure but causes renal failure, whereas the vasodepressor action of the clonidine analogue AL-12 occurs without detriment to renal function. These findings imply that angiotensin II receptor antagonists could lead to renal failure if used as antihypertensive agents in renovascular hypertension whereas this would be avoided with the use of clonidine-like analogues.

Matched MeSH terms: Acute Kidney Injury/etiology*; Acute Kidney Injury/physiopathology
Fulltext Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific association for the study of the liver (APASL): an update

Sarin SK, Choudhury A, Sharma MK, Maiwall R, Al Mahtab M, Rahman S, et al.

Hepatol Int, 2019 Jul;13(4):353-390.
PMID: 31172417 DOI: 10.1007/s12072-019-09946-3

The first consensus report of the working party of the Asian Pacific Association for the Study of the Liver (APASL) set up in 2004 on acute-on-chronic liver failure (ACLF) was published in 2009. With international groups volunteering to join, the "APASL ACLF Research Consortium (AARC)" was formed in 2012, which continued to collect prospective ACLF patient data. Based on the prospective data analysis of nearly 1400 patients, the AARC consensus was published in 2014. In the past nearly four-and-a-half years, the AARC database has been enriched to about 5200 cases by major hepatology centers across Asia. The data published during the interim period were carefully analyzed and areas of contention and new developments in the field of ACLF were prioritized in a systematic manner. The AARC database was also approached for answering some of the issues where published data were limited, such as liver failure grading, its impact on the 'Golden Therapeutic Window', extrahepatic organ dysfunction and failure, development of sepsis, distinctive features of acute decompensation from ACLF and pediatric ACLF and the issues were analyzed. These initiatives concluded in a two-day meeting in October 2018 at New Delhi with finalization of the new AARC consensus. Only those statements, which were based on evidence using the Grade System and were unanimously recommended, were accepted. Finalized statements were again circulated to all the experts and subsequently presented at the AARC investigators meeting at the AASLD in November 2018. The suggestions from the experts were used to revise and finalize the consensus. After detailed deliberations and data analysis, the original definition of ACLF was found to withstand the test of time and be able to identify a homogenous group of patients presenting with liver failure. New management options including the algorithms for the management of coagulation disorders, renal replacement therapy, sepsis, variceal bleed, antivirals and criteria for liver transplantation for ACLF patients were proposed. The final consensus statements along with the relevant background information and areas requiring future studies are presented here.

Matched MeSH terms: Acute Kidney Injury/etiology
Effect of kidney ischemia/reperfusion injury on proliferation, apoptosis, and cellular senescence in acute kidney injury in mice

Sari FT, Sari FT, Sari FT, Arfian N, Sari DCR

Med J Malaysia, 2020 05;75(Suppl 1):20-23.
PMID: 32471965

INTRODUCTION: Kidney ischemia/reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). Kidney IRI demonstrated apoptosis of epithelial cells in acute phase followed by proliferation of interstitial cells in chronic episode, and cellular senescence may contribute to development of AKI, however, its occurrence within acute or chronic episodes is still not completely understood.
METHODS: Kidney IRI was performed with bilateral pediculus clamping in Swiss Background mice (3 months, 30-40g). Mice were euthanised on day one (I/R1, n=6), day eight (I/R8, n=6), and day twelve (I/R12, n=6) to exam acute and chronic episodes. Sham operation procedure was performed in the control. Tubular injury was assessed based on periodic acid- Schift (PAS) staining. Reverse transcriptase PCR (RT-PCR) was done to quantify mRNA expression of Bax, Bcl-2, and p16. Immunohistostaining (IHC) was performed to examine localisation of apoptosis (p53) and proliferation (Bcl-2).
RESULTS: RT-PCR analysis showed upregulation of mRNA expression of Bcl-2, Bax, and p16 (p<0.05). The data showed that ischemia/reperfusion induces upregulation of Bax (p=0.20), Bcl-2 (p=0.45), p16 (p=0.18). Apoptosis and proliferation occurred in the epithelial cells in acute episodes, but occurred in interstitial areas in chronic episodes.
CONCLUSIONS: Ischemia/reperfusion injury induces upregulation proliferation, apoptosis, and cellular senescence in acute kidney injury. Apoptosis reached its peak on day 1, proliferation on day 8, and cellular senescence on day 12.

Matched MeSH terms: Acute Kidney Injury/etiology*; Acute Kidney Injury/physiopathology*
Role of the renal sympathetic nervous system in mediating renal ischaemic injury-induced reductions in renal haemodynamic and excretory functions

Salman IM, Ameer OZ, Sattar MA, Abdullah NA, Yam MF, Najim HS, et al.

Pathology, 2010 Apr;42(3):259-66.
PMID: 20350220 DOI: 10.3109/00313021003631304

We investigated the role of renal sympathetic innervation in the deterioration of renal haemodynamic and excretory functions during the early post-ischaemic phase of renal ischaemia/reperfusion injury.

Matched MeSH terms: Acute Kidney Injury/etiology; Acute Kidney Injury/physiopathology*
Characterization of renal hemodynamic and structural alterations in rat models of renal impairment: role of renal sympathoexcitation

Salman IM, Ameer OZ, Sattar MA, Abdullah NA, Yam MF, Najim HS, et al.

J Nephrol, 2010 5 4;24(1):68-77.
PMID: 20437405 DOI: 10.5301/jn.2010.6

BACKGROUND: Renal sympathetic innervation plays an important role in the control of renal hemodynamics and may therefore contribute to the pathophysiology of many disease states affecting the kidney. Thus, the present study aimed to investigate the role of the renal sympathetic nervous system in the early deteriorations of renal hemodynamics and structure in rats with pathophysiological states of renal impairment.

METHODS: Anesthetized Sprague Dawley (SD) rats with cisplatin-induced acute renal failure (ARF) or streptozotocin (STZ)-induced diabetes mellitus (DM) were subjected to a renal hemodynamic study 7 days after cisplatin and STZ administration. During the acute study, renal nerves were electrically stimulated, and responses in renal blood flow (RBF) and renal vascular resistance (RVR) were recorded in the presence and absence of renal denervation. Post mortem kidney collection was performed for histopathological assessment.

RESULTS: In innervated ARF or DM rats, renal nerve stimulation produced significantly lower (all p<0.05, vs. innervated control) renal vasoconstrictor responses. These responses were markedly abolished when renal denervation was performed (all p<0.05); however, they appeared significantly higher compared with denervated controls (all p<0.05). Kidney injury was suppressed in denervated ARF, while, irrespective of renal denervation, renal specimens from DM rats were comparable to controls.

CONCLUSIONS: Renal sympathoexcitation is involved in the pathogenesis of the renal impairment accompanying ARF and DM, and may even precede the establishment of an observable renal injury. There is a possible enhancement in the renal sensitivity to intrarenal norepinephrine following renal denervation in ARF and DM rats.

Matched MeSH terms: Acute Kidney Injury/chemically induced; Acute Kidney Injury/pathology; Acute Kidney Injury/physiopathology*
Successful treatment of acute kidney injury secondary to haeme nephropathy in paroxysmal nocturnal haemoglobinuria with alkaline diuresis

Sakthiswary R, Das S, Fadilah SA

EXCLI J, 2012;11:198-203.
PMID: 27298607

Paroxysmal nocturnal haemoglobinuria (PNH) also known as 'Marchiafava Micheli syndrome' is a rare condition which can lead to both acute and chronic forms of renal failure through renal tubular haemosiderin deposition. A 45-year-old lady with underlying PNH, presented with complaints of fever, productive cough followed by dark coloured urine. Investigations revealed pancytopenia with a markedly raised creatinine from her baseline (from 65 mmol/L to 385 mmol/L) consistent with acute kidney injury (AKI). Renal biopsy confirmed the diagnosis of haeme nephropathy. The renal impairment improved rapidly and normalised over a period of 5 days with alkaline diuresis (AD). The patient did not require haemodialysis unlike most other reported cases of AKI secondary to haeme nephropathy in PNH. This is the second reported case of AKI in PNH which was successfully treated with AD alone emphasizing the role of AD as a promising therapeutic strategy in this condition.

Matched MeSH terms: Acute Kidney Injury
Colistin-associated nephrotoxicity among patients in intensive care units (ICU) of hospitals in Selangor

Rashizal Sazli MR, Syed Mohamed AF, Wan Mazuan WM, Ling SM, Mahmud A, Amin Nordin S

Med J Malaysia, 2017 04;72(2):100-105.
PMID: 28473672 MyJurnal

INTRODUCTION: The increasing trend of extensively drugresistant gram negative bacteria responsible for nosocomial infections has prompted resurgence colistin usage. Colistin-induced nephrotoxicity is a concern with disparity in the reported rates between previous studies. This study aims to evaluate colistin-induced nephrotoxicity among Malaysian population.
METHODS: The medical records of ICU patients receiving colistin therapy in Hospital Serdang and Hospital Sungai Buloh from 2010 to 2012 were retrospectively reviewed. Demographics data, treatment characteristic as well as culture result and creatinine level were documented. Nephrotoxicity was determined based on RIFLE criteria.
RESULTS: A total of 100 patients were included. Median daily dose, cumulative dose and duration of colistin therapy were 3.0 MIU (IQR: 4, range 1-12), 17.8 MIU (IQR: 31.5, range 2-180) and seven days (IQR: 4, range 1-30). Nephrotoxicity was found in 23% of the study population. All cases were reversible but marginally associated with higher mortality. No statistical association exist between age, gender and race as well as administration routes with nephrotoxicity by univariable analysis. The association of dose and duration with nephrotoxicity was also not significant by univariable analysis. After adjustment for confounders, statistical association between the independent variables and dependent variable remains not significant.
CONCLUSION: Lower dose and shorter duration in local settings contribute to lack of association between colistin therapy and nephrotoxicity in this study. Higher dosing regimen with loading dose application has been introduced in the latest National Antibiotic Guideline. Further evaluation of colistin-induced nephrotoxicity and potential risk factors is therefore warranted.

Matched MeSH terms: Acute Kidney Injury/chemically induced*
Fulltext Acute renal failure due to multiple bee stings--case reports

Ramanathan M, Lam HS

Med J Malaysia, 1990 Dec;45(4):344-6.
PMID: 2152058

This report deals with a father and his son who developed acute renal failure following multiple bee stings. The renal lesion in these patients appears to be due to rhabdomyolysis caused by the bee venom. The other mechanisms are also discussed. The need for clinicians to be aware of acute renal failure as a complication of bee stings is stressed.

Matched MeSH terms: Acute Kidney Injury/etiology*

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