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العنوان
ROLE of NEUTROPHIL GELATINASE ASSOCIATED LIPOCALIN as an EARLY BIOMARKER of ACUTE KIDNEY INJURY in CRITICALLY ill PATIENTS\
المؤلف
Ahmed, Ahmed Elsayed Basyuoni.
هيئة الاعداد
باحث / Ahmed Elsayed Basyuoni Ahmed
مشرف / Seif El-Islam Abd-Elaziz Shaheen
مشرف / Ahmed Mohammed El-Sayed El-Hennawy
مناقش / Abd-Alaziz Abd-Allah Abd-Alaziz
تاريخ النشر
2014.
عدد الصفحات
143p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
العناية المركزة والطب العناية المركزة
تاريخ الإجازة
1/1/2014
مكان الإجازة
جامعة عين شمس - كلية الطب - الرعاية المركزة
الفهرس
Only 14 pages are availabe for public view

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Abstract

SUMMARY AND CONCLUSION
AKI is characterized by a rapid (hours to weeks) decline in GFR and retention of nitrogenous waste products such as BUN and creatinine. The most recent definitions proposed by the Acute Dialysis Quality Initiative (ADQI), RIFLE and AKIN have been based on rises in serum creatinine or reductions in urine output. These definitions aimed to promote the earlier detection and recognition of AKI triggering appropriate treatment prior to progressive injury and kidney failure.
Based on RIFLE and AKIN criteria, up to 20% of hospitalized patients may develop AKI. 35%-40% of patients who are critically ill will develop AKI, 5% will develop sever AKI requiring RRT. Among the subgroup of patients who survive initial dialysis, less than 25% require long-term dialysis. Currently, the mortality rate for hospital-acquired AKI ranges between 40% up to 70% (in ICU more than non- ICU patients) and is directly correlated to the severity of the patient’s other disease processes.
The etiology of AKI in general may be due to decrease renal perfusion (pre-renal causes), injury to the kidney glomeruli, tubules or interstitium (intra-renal causes) or obstruction of urinary outflow (post-renal causes). However, in ICU about 80% of AKI is due to intra-renal causes mostly due to ATN.
 Summary and Conclusion
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A stepwise evaluation approach to the patient with AKI is recommended. A comprehensive history and thorough physical examination suggest the diagnosis in most patients and the probable cause which is important for further evaluation and management. Laboratory investigation like urine analysis, urinary indices or biomarkers and imaging investigations can be helpful in diagnosis of AKI and its etiology. Renal biopsy is reserved for patients in whom pre-renal and post-renal causes have been excluded and the cause of intrinsic renal AKI is unclear.
Many biomarkers have been evolved e.g IL-18,KIM-1and (NGAL). The aim of these biomarkers in AKI to diagnose AKI earlier, indicate the location of the injury, need for renal replacement therapy and monitor the response to interventions.
In experimental and clinical studies, NGAL is one of the most studied and promising biomarkers for early diagno- sis of AKI. There is increasing evidence that NGAL is not only a marker of AKI but also a predictive factor for severity, mortality and hospital stay.
Strategies for management of AKI in ICU include conservative measures and RRT. Conservative measures include optimization of hemodynamic status by appropriate fluid therapy, administration of vasopressors, nephrotoxic medications should be stopped, in addition to control of
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99
electrolytes and acidbase disturbances with proper nutrition and symptomatic treatment of different complications of AKI.
Regarding fluid therapy, usually use crystalloids while colloids are restricted to special situation where serum albumin is considerably low because there is no advantage of colloids over crystalloids in the outcome. The amount of fluid is best evaluated by the clinical condition of the patient and the response following fluid therapy and it is stopped when there is no response or manifestations of overload develop.
Regarding drugs use in AKI, no role of dopamine in AKI while fenoldopam has beneficial effect on AKI in ICU patients, other vasopressor drugs have limited role in special circumstances. Diuretics have no role in prevention or treatment of AKI but can be used under their conventional indications. New drugs as EPO, natriuretic peptides and statins have promising effect on management of AKI. RRT is better to be started early as supportive therapy in presence of progressive azotemia and oliguria rather than a rescue therapy for late manifestations or absolute indications of AKI but there are no agreed consensus on the optimal criteria for starting RRT and this need more studies to be standardized.
Different modalities of RRT are now available including IHD, SLED, PD and CRRT with its different varieties. However each modality has its advantages and disadvantages
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100
and there are many considerations in selection of certain modality but as general rule the best modality for patients of AKI in ICU is CRRT because these patients are usually hemodynamically unstable.
The prescribed dose should be assessed at each session for intermittent hemodialysis) and daily (for continuous RRT )to account for any measured shortfalls in delivered dose. A minimum dose of RRT, however, needs to be delivered for AKI: the best evidence to date supports the use of at least 35 ml/h/kg for CVVH, CVVHD, or CVVHDF, or 1.2 Kt/V daily IHD. RRT is stopped when the initial indication for dialysis has resolved, fluid balance has been established and signs of kidney function recovery are detected.
There are promising new therapies for AKI like bio- artificial kidney and hematopoietic stem cells for renal regeneration.