Acute Kidney Injury

Management Investigations are aimed at :

1- Determination of the volume status : 1- Defining whether the patient has acute or chronic uraemia.
2- Defining whether uraemia results from prerenal, renal or postrenal factors,
A) If Hypovolaemia and Hypotension : Once initial resuscitation has been performed : 3- Establishing the cause.
fluid intake should be : Urine
1- Should be corrected by replacement of IV fluid or blood
1- matched to urine output plus
Criteria for Urine specific Urine sodium
- Types of fluid : Balanced salt solutions, such as : distinction between : osmolality FENa BUN : Cr. ratio
2- 500 mL to cover insensible losses gravity (mmol/L)
1- Isotonic (0.9%) saline (mOsm/kg)
2- Ringer’s lactate preferable when large volumes of fluid resuscitation are required, in order to avoid hyperchloraemic acidosis Pre-Renal > 1.020 > 500 < 20 < 1% 30 : 1
- Monitoring : Renal < 1.010 < 350 > 40 > 1% 15 : 1
Prerenal & renal uraemia may coexist, excessive fluid may lead to volume overload with pulmonary oedema Monitoring of (CVP) .
2- Critically ill patients may require Inotropic drugs to restore effective blood pressure.(clinical trials do not support a specific role for low-dose
low dopamine) 17.16 Investigation of patients with established acute kidney injury
B) If Hypervolemia : (Signs: Peripheral oedema, Basal
asal crackles, Elevation of jugular venous pressure) : Urea and Compare to previous results. Chronically abnormal in CKD
1- Diuretic therapy , after the adequate circulating blood volume : Mannitol (0.5 g/kg) & furosemide (2–4
4 mg/kg) IV single dose creatinine
2- Severe fluid overload in the presence of marked oliguria or anuria is indication for dialysis. Electrolytes If potassium > 6 mmol/L, treat urgently
2- Correction of serum electrolytes : Calcium and Low calcium and high phosphate may indicate CKD
ECG changes s : Calcium low in rhabdomyolysis: measure creatine kinase
Hyperkalemia The earliest ECG change hyperkalemia is the appearance of peaked T waves followed by widening of QRS
phosphate
Hypercalcaemia in myeloma
• Skeletal muscle : intervals ST segment depression ventricular arrhythmias cardiac arrest. Albumin Low albumin in nephrotic syndrome (see urinalysis below)
weakness, flaccid Indications : Low albumin in sepsis: take blood cultures
paralysis, areflexia. Procedures should be initiated when the serum potassium value rises above 6.0 mEq/L . Full blood count Anaemia may indicate CKD or myeloma
• Smooth muscle : Treatment :
Clotting screen Anaemia and fragmented RBC on blood film with raised LDH in thrombotic microangiopathy
Intestinal colic, nausea, A) Stabilize cell membrane potential : Low platelets and abnormal coagulation in DIC, including in sepsis: take
take blood cultures
vomiting. - IV calcium gluconate (10 mL of 10% solution) C-reactive protein ESR is misleading in renal failure
• Cardiac muscle : B) Shift K into cells : High CRP may indicate sepsis or inflammatory disease
-ECG changes : " see " - Inhaled β2-adrenoceptor
adrenoceptor agonist (e.g. salbutamol) Urinalysis Less reliable in an oliguric catheterised patient
-Arrhythmias /cardiac arrest. - IV glucose (50 mL of 50% solu9on) and insulin (5 U Actrapid®) Seek earlier results if possible
- IV sodium bicarbonate if acidosis present. Marked haematuria suggests glomerulonephritis, tumour of renal tract or bleeding disorder
C) Remove K from body Heavy proteinuria suggests glomerular disease: measure PCR or ACR
- IV furosemide and normal saline Casts or dysmorphic red cells suggest glomerulonephritis
Urine microscopy
- Ion-exchange
exchange resin (e.g. Resonium®) orally or rectally Leucocytes suggest infection/interstitial nephritis
- Dialysis Crystals may be observed in drug-induced
drug or uric acid nephropathy
- Dilutional disturbance corrected by fluid restriction rather than NaCl administration.
Hyponatremia - Administration of hypertonic (3%) saline should be limited to patients with :
Renal ultrasound Hydronephrosis enlarged bladder in urinary tract obstruction: consider
ider PSA and further imaging.
Small kidneys suggest CKD
1- Symptomatic
ymptomatic hyponatremia (seizures, lethargy) or Asymmetric kidneys suggest renovascular or developmental disease: consider renal artery imaging
2- Serum sodium level <120 mEq/L. Culture blood, urine, sputum, wounds as appropriate
Cultures
Hypocalcemia & - lowering the serum phosphorus by : Treat all infections
1- Dietary
ietary phosphorus restriction and Pulmonary oedema in fluid overload
Hyperphosphatemia Chest X-ray
2- Administration
dministration of phosphate binders (calcium acetate and calcium carbonate). Globular heart in pericardial (uraemic) effusion: perform echocardiogram
echocardio
Symptomatic hypocalcemia (tetany) can be treated with IV calcium; it must be given cautiously. HIV and hepatitis serology is urgent if dialysis is needed
Serology
Restoration of blood volume will correct acidosis by restoring kidney function
ECG If patient is > 40 yrs or has electrolyte abnormali9es or risk of cardiac disease
- Indications of treatment : 1- If acidosis is severe (arterial pH <7.15; serum bicarbonate <8 mEq/L)
Metabolic acidosis
2- contributes to hyperkalemia.
Rarely requires TTT - Treatment:
1- NaHCO3 IV,, to raise arterial pH to 7.20 (which approximates a serum HCO3 level of 12 mEq/L).
emainder of the correction by oral after normalization of the serum Ca & phosphorus levels.
2- Remainder
Renal AKI
3- ARF patients are predisposed to gastrointestinal bleeding : Factors that can help differentiate the various causes of
• Causes: Because
ecause of uremic platelet dysfunction, increased stress, and heparin exposure if on hemodialysis renal and post-renal AKI are summarised in :
• Treatment: Oral or IV H2 blockers as: ranitidine.
4- Hypertension :
• Cause : 1- may result from hyperreninemia associated with the primary disease process and/or
2- expansion of the extracellular fluid volume and is most common in ARF patients .
• Treatment: Salt & water restriction + Diuretic administration:
1- Severe symptomatic hypertension continuous infusions of sodium nitroprusside .
2- Longer acting agents such as for maintaining control of BP.
5- Anemia :
• The anemia of ARF is generally mild (Hb 9–1010 g/dL) and primarily results from volume expansion (hemodilution).
• Slow (4–66 hr) transfusion with packed red blood cells (10 mL/kg) diminishes the risk of hypervolemia.
• The use of fresh, washed red blood cells minimizes the risk of hyperkalemia.
6- Infection :
• Patients
nts with AKI are at substantial risk of intercurrent infection because humoral and cellular immune mechanisms are depressed.
• Clinical examination + microbiological investigation, is required to diagnose infection treated promptly .
7- Neurological symptoms: include: headache, seizures, lethargy, and confusion.
• Causes: hyponatremia, hypocalcemia, hypertension, cerebral hemorrhage, cerebral vasculitis, and uremic state.
• Treatment: Diazepam is the most effective agent in controlling seizures
8- Nutritional : - Na, K,, phosphorus should be restricted. /Protein intake should be restricted moderately while
- Maximizing
aximizing caloric intake to minimize the accumulation of nitrogenous wastes
9- Renal Replacement Therapy : 2 main options for RRT in AKI are : 1- haemodialysis 2- high-volume volume haemofiltration,, indications:
Clinical Laboratory
• Acute Pulmonary edema. B. Laboratory :
• Pericarditis. • Urea : > 200 mg/dl ( N : 20 - 40 mg/dl )
• Persistent diarrhea. • Crea9nine : > 8 mg/dl , > 7 in DM ( N : 0.7 - 1.2 mg/dl )
• Preoperative. • K : > 7 mEq/L . ( N : 3.5 - 5.5 mEq/L )
• Coma. • HCO3 : < 14 mEq/L .
• Convulsion • PH : < 7.2
• Deterioration of general health. • Hypercatabolic RF : - Creatinine by > 1mg/d.
- K by > o.8 mEq/d.
 Chronic renal failure
The aims of management in CKD are to : Blood : Suggested investigations in chronic kidney disease
1- Prevent or slow further renal damage Urea and To assess stability/progression: compare to
2- Limit
imit adverse physiological effects of renal impairment on skeleton & haematopoiesis 1- Anemia : creatinine previous results
3- Treat risk factors for cardiovascular disease; • Anaemia is common in patients with
h a GFR below 30 mL/min/1.73 m2. Urinalysis and Haematuria and proteinuria
uria may indicate cause.
quantification Proteinuria indicates risk of progressive CKD
• Regimens : of proteinuria requiring preventive ACE E inhibitor
inhibito or ARB therapy
1- Diet & lifestyle Modifications : 1- Recombinant human erythropoietin ( Eprex ) : 4000 u 2 9mes / week.
2- Packed RBCs.
Electrolytes
Calcium, phosphate,
To identify hyperkalaemia and acidosis

Diet : parathyroid hormone Assessment of renal osteodystrophy

• Target :
1- Preventing excessive
xcessive consumption of protein. and 25(OH)D
The target haemoglobin is usually between 100 and 120 g/L (10–20
(10 g/dL). Albumin Low albumin: consider malnutrit
alnutrition, inflammation
2- Ensuring
uring adequate calorific intake.
FBC (± Fe, ferritin, If anaemic, exclude common non-renal
non
3- Limiting potassium & phosphate intake.
4- Limiting excessive water intake to avoid body water retention. Renal bone disease folate, B12) explanations then manage as renal anaemia
Lipids, glucose ± Cardiovascular risk high in CKD: treat risk factors
Life style : 1- Treatment should be initiated with active vitamin D metabolites , either : HbA1c aggressively
1- Stop smoking: this a) slows decline in renal function b)reducing cardiovascular risk. • 1-α-hydroxyvitamin D or Only if there are urinary symptoms (to exclude
• 1,25- dihydroxyvitamin D obstruction) or progressive CKD.
2- Exercise and weight loss may also reduce proteinuria and have beneficial effects on Renal ultrasound Small kidneys suggest chronicity.
cardiovascular risk profile. - Indications : patients who are found to have : Asymmetric renal size suggests renovascular or
• Hypocalcaemia or developmental disease
2- Medications : • Serum
erum PTH levels more than twice the upper limit of normal. Hepatitis and HIV If dialysis or transplant is planned. Hepatitis B
serology vaccination recommended if seronegative
Cardiovascular : - The dose should be adjusted to try to reduce PTH levels to between 2 and 4 9mes the ECG If patient is > 40 yrs or hyperkala
yperkalaemic, or there are
risk factors for cardiac disease
upper limit of normal to avoid over-suppression
suppression of bone turnover.
1- Anti-hypertensives :
Investigations
1- Slows the rate at which renal function declines in CKD • The recommended investigations in patients with CKD are shown in
2- Lowering the risk of hypertensive heart failure, stroke and peripheral vascular disease, 2- Hyperphosphataemia :
• Their main aims are:
3- Reducing proteinuria 1) Dietary
ietary restriction of foods with high phosphate content (milk, cheese, eggs ) 1- to identify the underlying cause where possible, since this may
2) Phosphate-binding drugs : influence the treatment.
• Targets: • Calcium carbonate / Aluminium hydroxide / Lanthanum carbonate / 2- to identify reversible factors that may worsen
orsen renal
ren function, such as
- 130/80 mmHg for uncomplicated CKD, Polymer-based
based phosphate binders such as sevelamer hypertension, UTI, nephrotoxic drugs, and d salt and
an water depletion.
- 125/75 mmHg for CKD complicated by significant proteinuria of more than 1 g/day. 3- to screen for complications of CKD.
• Aim: 4- to screen for cardiovascular risk factors.
• Regimen : - maintain serum phosphate values at 5.6 mg/dL or below .
- ACEIs, methyl dopa , β blocker , Caa channel blocker or Diuretic. Referral to a nephrologist :
Criteria for referral of chronic kidney disease patients to a nephrologist :
3- Hyperparathyroidism : • Age < 40 years
2- Lipid-lowering
lowering therapy (Statins) : 1) ttt of renal osteodystrophy • Stage 4 CKD or worse (eGFR < 30 mL/min/1.73 m2)
• Hypercholesterolaemia is almost universal in patients with significant proteinuria
proteinuria,, and 2) Parathyroidectomy may required for the treatment of 3ry hyperparathyroidism. • Rapid deterioration in renal function1
increased triglyceride levels are also common in patients with CKD. 3) Calcimimetic agents, such as cinacalcet : • Significant proteinuria (PCR > 100 mg/mmol or ACR > 70 mg/mmol)
• Significant haematuria:
- which bind to the calcium-sensing
sensing receptor and reduce PTH secretion.
• Effect : - After exclusion of urinary tract infection and urological abnormalities
- They have a place if parathyroidectomy is unsuccessful or not possible. such as stones and tumours.
1- Lipid lowering shown to reduce vascular events in non
non-dialysis CKD patients.
2- Control of dyslipidaemia with statins may slow rate of progression of renal disease.
Maintaining fluid and electrolyte balance :
3- Reduction of proteinuria : 1- Patients with evidence of fluid retention :
• There is a clear relationship between the degree of proteinuria and the rate of
1) Dietary
ietary sodium intake limited to about 100 mmol/day.
mmol/day
progression of renal disease,, and strong evidence that :
2) Loop
oop diuretics may also be required to treat fluid overload.
reducing proteinuria reduces the risk of progression.
1- Angiotensin-converting
converting enzyme (ACE) inhibitors and 2- If hyperkalaemia occurs :
2- angiotensin II receptor blockers (ARBs) 1) Drug
rug therapy should be reviewed, to reduce or stop potassium-sparing
potassium diuretics,
ACE inhibitors and ARBs.
• Effect:
1- Reduce
educe proteinuria and retard the progression of CKD due to the reduction 2) Correction of acidosis may be helpful,
in blood pressure. 3) Limi9ng
imi9ng potassium intake to about 70 mmol/day may be necessary in late CKD.
2- Reduce the risk of cardiovascular events .
binding resins, such as calcium resonium, may be useful in the
4) Potassium-binding
• Treatment with ACE inhibitors and ARBs accompanied by an immediate reduction in short term but should not be used chronically.
GFR when treatment is initiated, due to a reduction in glomerular perfusion pressure.
3- Bicarbonate :
• Treatment can be continued so long as reduction in GFR is < 20% and is not progressive.
progressive • Should
hould be maintained above 22 mmol/L
• Accordingly ACE inhibitors and/or ARBs should be prescribed to all patients with • by giving NaHCO3 supplements (star9ng dose of 1 g 3 9mes daily, increasing as required).
diabetic nephropathy and those with proteinuria, irrespective of whether or not
• If the increased sodium intake induces hypertension or oedema :
hypertension is present (providing
providing that hyperkalaemia does not occur
occur).
calcium carbonate (up to 3 g daily) may be used as an alterna9ve, since this has
the advantage of also binding dietary phosphate.
phosphat