Acute kidney injury (AKI), previously known as acute

renal failure (ARF) is characterized by sudden loss of the ability of the kidneys to excrete wastes, concentrate urine, conserve electrolytes, and maintain fluid balance.

Robert W. Schrier, Wei Wang, Brian Poole, and Amit Mitra, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado, USA-Acute renal failure: definitions, diagnosis, pathogenesis, and therapy, The Journal of Clinical Investigation http://www.jci.org Volume 114 Number 1 July 2004

The Caribbean Renal Registry 2007 showed that the commonest causes of ESRD are HTN (65.5%) , DM (27.6%) and chronic GN (12.5%) .
A study done at EWMSC in determining trends in the prevalence of ESRD between 1999-2007 showed that the most affected were males, aged 50-59, who were HTN and/or diabetic and of African descent.

AK Soyibo; EN Barton, Caribbean Institute of Nephrology, Department of Medicine, The University of the West Indies and the University Hospital of the West Indies, West Indian med. j. vol.56 no.3 Mona June 2007 Mungrue K, Ramdial S, Barran A, Lorinda B, Bridgelal A, Gildharie S, Leeloy J, Mohammed O, Ragbir T, Rampersad R, Ramtahal R, Suratsingh N, The epidemiology of end stage renal disease at a centre in Trinidad, West Indian Med J. 2011 Oct;60(5):553-6.

Rise in SCr or BUN concentration

Inadequate renal plasma flow and low intraglomerular hydrostatic pressure to support normal GF.

Clinical conditions associated wit pre-renal azotemia- hypovolemia, decreased cardiac output, medications that interfere with renal autoregulatory responses e.g. NSAIDS, angiotensin 2 inhibitors
The decreased renal plasma flow leads to ischemic injury or ATN.

Acute Kidney Injury; Harrisons Principles of Internal Medicine, 18e; Chapter 279

Acute blockage (partial or total) to undirectional urine flow leads to increased

retrograde hydrostatic pressure and interference with GF.

Causes: Bladder neck- BPH, prostate cancer, neurogenic bladder, anticholinergic drugs Ureteric blockage- blood clots, calculi, neoplasia, retroperitoneal fibrosis Lower tract obstruction- blood clots, strictures, calculi

Acute Kidney Injury; Harrisons Principles of Internal Medicine, 18e; Chapter 279

Comorbodities- HTN, DM, CCF, Multiple myeloma, autoimmune diseases, connective

tissue diseases, myeloproliferative disorders. Acute onset fatigue, weight loss, nocturia, sleep disturbance, pruritus. Pre-renal failure- hypovolemia, thirst, dizziness, orthostatic hypotension, vomiting, diarrhoea, blood loss, signs of CCF e.g. PND, orthopnoea. Intrinsic AKI- hematuria, edema, hypertension, muscular pain (rhabdomyolysis), drug history. Post-renal failure- BPH (hesitancy, urgency, strangury, polyuria), flank pain, drug history e.g. chemotherapy, hematuria

Acute Kidney Injury Clinical Presentation Author: Biruh T Workeneh, MD, PhD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN; Medscape; http://emedicine.medscape.com/article/243492-clinical

CBC- anaemia due to hemolysis, thrombotic microangiopathy, thrombocytopenia

RFTs- hyperkalemia, hyperphosphatemia, hypocalcemia, elevated uric acid, CK, SCr, BUN elevation ESR, CRP

LFTs and hepatits serology of dialysis is considered

Blood cultures if septic C3/C4 levels Autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM Biomarkers for AKI- alpha-1 microglobulin, retinol binding protein, kidney injury molecule-1 (KIM-1), interleukin-18

Acute Kidney Injury; Harrisons Principles of Internal Medicine, 18e; Chapter 279

Rinaldo Bellomo,

Claudio Ronco,

John A Kellum,

Ravindra L Mehta,

Paul Palevsky,

and the ADQI workgroup

Rinaldo Bellomo, Claudio Ronco, John A Kellum, Ravindra L Mehta, Paul Palevsky, Acute renal failure definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group the ADQI workgroup, Crit Care. 2004; 8(4): R204R212 Published online 2004 May 24.

Ravindra L Mehta, John A Kellum, Sudhir V Shah, Bruce A Molitoris, Claudio Ronco, David G Warnock, Adeera Levin, and the Acute Kidney Injury Network; Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury; Crit Care. 2007; 11(2): R31. Published online 2007 March 1.

Uremia Hyper/hypo-volemia Hyponatremia Hyperkalemia Acidosis Hyperphosphatemia and hypocalcemia Bleeding- DIC, sepsis, platelet dysfunction due to uremia Anaemia- AKI-related uremia causes decreased erythropoesis Infections Cardiac complications-arrhythmias, pericarditis, pericardial effusions Malnutrition- hypercatabolic state

Acute Kidney Injury; Harrisons Principles of Internal Medicine, 18e; Chapter 279

Current treatment for AKI is mainly supportive ( dopamine, fenoldopam, mannitol

may be harmful to the patient)

Maintenance of volume homeostasis and correction of biochemical abnormalities are the main goals.

Treat the precipitating cause e.g. sepsis, blood loss etc. Stop nephrotoxic agents Monitor patients BP, pulse, urine output, daily fluid balance and weight charting-

look for signs of hypervolemia e.g. gallop rhythm, increased BP and JVP,
crepitations and edema

Due to malnutrition complications, high calorie diet (2000-4000cal/day) is

indicated with high quality protein; fluid and salt restriction. Hyperkalemia- ECG changes show tall tented T-waves, flat p-waves, increased PR interval, wide QRS complex treated with 10% 10ml calcium gluconate IV over 2 mins, 50ml 50& dextrose with 10U of rapidly acting insulin IV over ~30mins.

Furosemide can be used if there is pulmonary edema

Indications:

Refractory pulmonary edema Persistent hyperkalemia (>7 mmol/L) Severe metabolic acidosis (pH< 7.2 or base excess <10) Uremic encephalopathy Uremic pericarditis