A Nurse Is Reviewing the Urinalysis Report of a Client Who Has Acute Glomerulonephritis
Ulster Med J. 2014 Sep; 83(3): 149–157.
Prevention and Management of Acute Kidney Injury
Introduction
Astute Kidney Injury (AKI) is common, expensive to manage, prolongs hospitalization and is associated with increased mortality. In 2009 the National Confidential Enquiry into Patient Consequence and Death (NCEPOD) published a written report into the intendance of patients who died with a diagnosis of AKIi. But 50% of patients were accounted to accept had a 'good" standard of care. The NCEPOD written report identified inadequate assessment of patients at take a chance of AKI and deemed lx% of post-admission AKI was predictable and 21% was avoidable. Two thirds of patients had a meaning level of AKI earlier a diagnosis was fabricated and there was inadequate senior review of these patients. More severe AKI is associated with higher mortality. The in-hospital bloodshed rate for AKI has been reported at 24% and increases with more severe AKI2. In Northern Republic of ireland, an audit of patients with severe AKI requiring dialysis demonstrated a 90 day mortality charge per unit of up to 40% (personal communication) In 2013, the National Institute for Health and Care Excellence (NICE) published guidance on AKI3. Prissy have calculated that if AKI was recognized and treated with attention to hydration and medication, 100,000 cases could exist prevented and up to 42,000 deaths avoided annually. The National Clinical Director for Kidney4 care has stated that management of AKI tin provide a barometer past which nosotros tin measure and improve the intendance of the acutely unwell patient whatever the underlying cause. There is clearly a need for all clinicians to be competent in managing this common condition. The aim of this One thousand Rounds article is to provide applied information on prevention and management of AKI.
Definition of Aki
The term AKI has replaced that of Acute Renal Failure.
This is to recognize that there are varying degrees of kidney injury severity and to encourage early on identification and management of AKI.
AKI is defined past an acute reduction in kidney function as identified by an increment in the serum creatinine and reduction in urine output.
The severity of AKI is reflected by the AKI stage5 AKI 1 - 3 (Table 1), with Stage 1 defined as a ascension of serum creatinine of >26 umol/L or 1.v to 1.9 times the baseline serum creatinine. Such small serum creatinine elevations are associated with increasing mortalityhalf dozen providing a rationale for the inclusion of this apparently small rise in serum creatinine in the AKI staging scheme.
Table 1
Kidney Disease Improving Global Outcomes (KDIGO) staging nomenclature for AKI
| Kidney Illness Improving Global Outcomes (KDIGO) staging classification for AKI | ||
|---|---|---|
| Stage | Serum creatinine (Scr) criteria | Urine output criteria |
| 1 | Ascension in Scr of 26 umol/L within 48 hrs Increase of 1.5 – ane.9 x baseline Scr within past vii days | < 0.5 mL/Kg/hr for > 6 consecutive hours |
| ii | Increment of 2 - 2.9 x baseline Scr | < 0.v mL/Kg/hr for > 12 consecutive hours |
| 3 | Increment of 3 x baseline Scr or Scr > 354 umol/Fifty or Commenced on dialysis | |
| Additional Burglarize Criteria reflecting outcome of AKI | ||
| Loss | Need for ongoing dialysis for > 4 weeks | |
| Failure | Need for ongoing dialysis for > 3 months | |
In that location are too two outcome stages - Loss and Finish Stage Renal Disease (ESRD)vii. These stages recognize that AKI can subsequently atomic number 82 to chronic kidney disease (CKD) and ESRD requiring long term dialysis (Figure ane). Studies in the diabetic population8 take shown that episodes of AKI double the risk of patients developing Stage four CKD (estimated GFR 15 – 29 mL/min/1.73m2). Recent NICE Guidelines on CKD recommend monitoring of all patients who recover renal function post-obit an episode of AKI for a minimum of ii years to ensure early on detection and management of CKD3.
Potential outcomes following episode of Acute Kidney Injury
It is important to appreciate that the serum creatinine does not accurately reflect the Glomerular Filtration Rate (GFR) in a patient who is non in steady state. The serum creatinine is influenced by creatinine generation, volume of distribution and excretion. Thus a sudden autumn in GFR is accompanied by a irksome rise in serum creatinine which plateaus at between seven and 10 days when creatinine production equals creatinine excretion. Big changes in GFR are initially manifested equally small changes in serum creatinine. This may lead to a delay in recognizing the degree of AKI in a patient demonstrating an initial "minor" rise in serum creatinine. Similarly, during recovery from AKI, the serum creatinine may lag backside renal recovery.
Eastward-Alarm for Acute Kidney Injury
A national algorithm, standardizing the definition of AKI, has at present been agreed for employ in Northern Ireland. This has been integrated into the Regional Laboratory system Audit Implementation Network (Proceeds world wide web.gain-ni. org) Acute Kidney Injury Algorithm (Effigy 3). This alert will automatically place patients with AKI and enhance clinicians' ability to recognize AKI and instigate early on handling.
Northern Ireland GAIN AKI Algorithm
Causes of Aki
AKI is common with a recent report reporting an incidence of 25% in unselected medical admissions9. It is of import to recognize that ii thirds of episodes of AKI develop prior to the hospital admission. This affords an important opportunity to identify and prevent AKI in at risk patients.
For clarity the causes of AKI have been divided into three groups; Pre-renal, Intrinsic-renal and Mail-renal. Tabular array 2 lists some mutual causes.
Table 2
Causes of AKI
| Pre-renal (hypoperfusion) | Intrinsic-renal | Post-renal Volume depletion |
|---|---|---|
| Volume depletion | Astute Tubular Injury | Bladder outlet obstruction |
| • Dehydration | Interstitial nephritis | Bilateral ureteric obstruction. |
| • Blood loss | Glomerulonephritis | Obstruction of a single performance kidney. |
| Hypotension | Vasculitis | |
| • Sepsis | ||
| • Medications | ||
| • Cardiac failure |
In reality the majority of causes of AKI are not renal specific. The kidneys receive 25% of the cardiac output at rest are therefore sensitive to any systemic upset. In the largest trial of patients admitted to ICU with astringent AKI10 the most common causes (often in combination) were septic shock (47%), post major surgery (34%), cardiogenic shock (27%), and hypovolaemia (26%). Deterioration in kidney office should provoke careful inspection for the common causes of haemodynamic compromise and sepsis throughout the trunk. Only when pre-renal causes accept been excluded should specific attention return to consideration of intrinsic renal affliction and renal tract obstruction.
Pathophysiology of Pre-Renal Aki and Acute Tubular Necrosis (ATN)
Well perfused, healthy kidneys will produce on average 180 Fifty of glomerular filtrate per twenty-four hour period, the majority of which is reabsorbed leading to a usual excretion of 1.v - 2 L of urine. Production of this volume of filtrate is dependent on an adequate glomerular capillary pressure level which is the driving force for filtration. Normal glomerular capillary pressure is maintained past afferent arteriole vasodilation and efferent vasoconstriction. This mechanism is known every bit renal autoregulation. The ability to maintain renal haemodynamics becomes impaired at a renal arterial pressure level below 70 mmHgeleven. When this occurs the GFR will fall in proportion to farther reduction in claret pressure. The GFR will stop when the renal arterial claret pressure is < l mmHg.
A reduction in renal perfusion due to hypotension results in prostaglandin mediated dilation of the afferent renal arteriole and constriction of the efferent glomerular capillary mediated by angiotensin 2. However in patients with impaired autoregulation the GFR volition fall even if the hateful arterial pressure remains inside the normal range.
Factors which increment susceptibility to renal hypoperfusion are listed in Table 3.
Table 3
Factors increasing susceptibility to renal hypoperfusion
| Failure to decrease arteriolar resistance |
|
| Failure to increase efferent arteriolar resistance |
|
| Renal avenue stenosis |
With prompt restoration of intravascular volume and blood pressure, normal renal haemodynamics can be restored resulting in complete recovery of renal function.
Nevertheless, in the face of persisting hypoperfusion, endogenous vasoconstrictors increase afferent arteriolar resistance. Causes of a depression perfusion state are shown in Table 4.
Table 4
Causes of Renal Hypoperfusion
Hypovolaemia
|
Cardiac causes
|
Reduced peripheral vascular resistance
|
Local renal hypoperfusion
|
Renal hypoperfusion reduces glomerular capillary pressure level and the GFR. The post-glomerular capillary bed which perfuses the tubules will too have diminished claret menstruum leading to a subsequent ischaemic structural injury to the renal tubules often referred to equally ischaemic Astute Tubular Necrosis (ATN)12. This state is characterized by a rising serum creatinine and a reduced urine volume refractory to further increases in intravascular volume and renal perfusion pressure. Management of this state includes avoidance of fluid overload, maintenance of an adequate mean arterial pressure (> 65 mmHg), correction of electrolyte disorders (potassium) and treatment of the underlying precipitating condition. Such patients may require a temporary period of dialysis support.
AKI in hospitalized patients tin can be thought off every bit a two striking procedure. Susceptibility factors create an access patient grouping vulnerable to a subsequent 'second hit' - hypoperfusion events13. This can be seen in studies of AKI in critically sick patientsx where the median length of inpatient stay prior to the development of severe AKI is v days. This filibuster is an opportunity to both forestall and reduce the severity of AKI in hospitalized patients.
Prevention of Aki
Community Caused
Patients in the customs with CKD (eGFR < 60 mL/ min/1.73mii) and patients with normal renal function who are treated with an ACE inhibitor (ACEi) or angiotensin receptor blocker (ARB) are at increased risk of AKI if they develop an illness associated with hypovolaemia and hypertension. Such patients tin be identified, educated and issued with a Kidney Care Card (Figure 4). This provides instructions for temporary abeyance of sure medications, which may in this setting, induce, exacerbate and complicate AKI. These drugs can be remembered by the mnemonic DAMN (diuretics, ACEi/ ARBs, metformin, NSAIDs).
Community Kidney Care Card
Hospitalised patients
Prevention of AKI should follow the following principles;
Risk Assessment
All patients, both on admission and during their infirmary stay should be assessed regularly for their risk of developing AKI. Figure 5 gives an example of a take chances cess tool used in the Southern Health and Social Care Trust. NICE have identified the following patient groups (Table v) who require special attending.
Example of an admission AKI take chances cess tool
Table five
Patients at risk of AKI
| Age over 65 years |
| Existing CKD (eGFR < lx mL/min/1.73m2), Previous episode(southward) of AKI |
| Co - Morbidity (Cardiac / Liver failure, Diabetes Mellitus |
| Use of nephrotoxic drugs (Diuretics, ACEi/ARBs, NSAIDs) |
| Diagnosis of sepsis |
| Hypovolaemia / Hypotension / Oliguria (< 0.5 mL/kg/hr) |
| Deteriorating Early Warning Scores |
| Symptoms / history or condition that may lead to urinary tract obstacle |
| Use of iodinated dissimilarity agents inside the previous week |
Perioperative AKI is common. Recognition of patients who are at take a chance will permit measures to be undertaken to reduce exposure to renal insults and maximize renal recovery should AKI occur14. An like risk assessment tool for use in Surgical patients is shown in Figure half-dozen.
Example of a Surgical AKI risk assessment tool
Optimisation of fluid remainder
Fluid volume status should be carefully assessed with respect to both fluid depletion and fluid overload. Patients at risk of dehydration due to prohibited or poor oral intake should be prescribed maintenance IV fluids.
Optimisation of blood pressure level
Hypotension systolic claret pressure (SBP) <110 mmHg / hateful arterial pressure (MAP) < 65 mmHg) needs urgent cess and handling with Iv fluid challenges and vasopressor agents where indicated.
Medication review
Temporary abeyance of ACEi and ARBs is appropriate in patients with dehydration, hypotension (systolic blood pressure level < 110 mmHg) and / or deteriorating renal function. In patients who continue to exist prescribed ACEi or ARBs, alteration of timing of drug prescription to 6 pm volition allow acceptable time to assess clinical state and review their renal function in instance there is a need to temporarily hold these medications.
Where clinically indicated aminoglycosides can continue to be used paying careful attention to renal function and drug levels.
Reducing the risk of dissimilarity induced AKI
AKI secondary to radiological contrast media typically occurs within 72 hrs of receiving such agents. The risk of dissimilarity nephropathy can be reduced by temporary abeyance of potentially nephrotoxic medication and acceptable book expansion (Table 6)
Tabular array half dozen
Prevention of Contrast Nephropathy
| Identify risk | • eGFR < 30 mL/min/one.73m2 • eGFR 30 - 60 mL/min/1.73m2 and risk factors (Tabular array 5) |
| Manage risk | • Hydration - Iv 1.4% sodium bicarbonate / 0.9% saline at 3 mL/kg/hr 1hr pre and 1 mL/kg/hr for 6hrs post process • Omit potentially nephrotoxic medications (ACEi/ARBs / NSAIDs / metformin on day of process and do non restart until renal function stable at 48 - 72 hrs • Utilise low osmolar agents in the lowest dose. • Recheck renal part 48 - 72 hrs following the procedure |
Assessment of Aki
Clinical assessment
This should brainstorm with a search for the cause of AKI focusing on clinical evidence of hypoperfusion states (volume depletion and hypotension) and urinary tract obstruction. AKI in the setting of resistant hypotension suggests significant underlying sepsis, the source of which may not be immediately apparent especially in cases of intra-abdominal sepsis.
Intrinsic renal illness in the class of vasculitis may present with a typical rash, uveitis and / or arthropathy. Intrinsic renal disease should always be considered where AKI is occurring in the absence of significant aridity, hypotension and obstruction.
The effect of AKI should as well be assessed, paying particular attending to evidence of volume overload - frequently manifest by peripheral and pulmonary oedema and increasing oxygen requirements. In severe AKI (Phase 3) pericarditis and encephalopathy may be present.
Dipstick urinalysis is function of the clinical assessment and should be done equally soon as urine is available for testing. Hypoperfusion states are suggested past a raised urine specific gravity (> 1.020). In the absence of haemodynamic upset and sepsis, the presence of claret and protein in the urine should prompt consideration of a vasculitis / glomerulonephritis rather than a urinary tract infection.
Laboratory and Radiological Investigations
The GAIN AKI Algorithm (Figure 3) lists the required investigations.
In patients suspected of underlying sepsis, a serum lactate and arterial blood gas are essential in defining the severity of the metabolic upset.
Where at that place is no obvious precipitating factor for AKI, a renal immunology screen (including antineutrophil cytoplasmic antibodies (ANCA), anti-glomerular basement membrane antibodies (anti-GBM), serum electrophoresis and serum free light chains) should be sent urgently as the clinical management of such cases requires prompt specialist handling.
In addition the finding of AKI, anaemia and thrombocytopenia with a normal coagulation profile should prompt a search for haemolysis (claret film, haptoglobulins) which occurs in Haemolytic Uraemic Syndrome, cancerous hypertension, scleroderma and pre-eclampsia.
A chest x-ray can provide both bear witness of a cause (pneumonia, pulmonary shadowing in vasculitis) and also help evaluate potential volume overload.
Renal tract ultrasound should exist done inside half dozen hours where obstruction is considered. The presence of bilateral hydronephrosis and an empty bladder will require an urgent non-contrast CT scan to identify retroperitoneal obstruction to the ureters.
The presence of AKI should not forestall the use of contrast enhanced CT scanning to diagnose the source of sepsis, peculiarly if a surgically remediable condition (intraabdominal abscess, ischaemic bowel) is being considered.
Management of Established Aki
Restore Renal Perfusion
Equally the majority of cases of AKI occur in association with volume depletion and sepsis, information technology is essential to restore effective renal perfusion equally soon every bit possible. This will allow early recovery of renal function and aid to avoid the development of astute tubular necrosis.
Optimise intra-vascular fluid volume
Volume status should exist carefully assessed and an attempt should be made to categorise the patient into ane of iii states; hypovolaemic, euvolaemic or hypervolaemic.
Hypovolaemic patients may have clinical signs of aridity, are oliguric (urine output < thirty mL/hour) often with a full-bodied urine (Specific Gravity > 1.020)
There is no gilt standard to definitively identify dehydration. However, hypotension (SBP < 110 mmHg), a postural fall in blood force per unit area with increment in center rate, reduction in peripheral perfusion / skin turgor and dry mucous membranes are indicative signs.
Hypovolaemia should exist promptly corrected with repeated boluses of 250 - 500 mL of crystalloid up to an initial total of 2 litres over two hours.
Hartmann's solution or 0.9% sodium chloride solution should exist used. Hartmann'south solution contains a small-scale corporeality of potassium (v mmol/L) and should exist avoided in patients with pregnant hyperkalaemia (Potassium > 6 mmol/L). Large volumes of 0.ix% sodium chloride can provoke a hyperchloraemic metabolic acidosis.
Failure of the patient to maintain an constructive claret pressure following this authorities should heighten the possibility of underlying sepsis or significant ongoing losses. Both these latter scenarios require senior assessment rather than continuing to prescribe increasing large volumes of fluid in the face of poor urine output. Fluid accumulation resulting in a positive fluid residual is a frequent event in critically ill patients with AKI. Such fluid accumulation (> 10% fluid weight gain) is independently associated with increased mortality15 fails to ameliorate renal function and is associated with worsening respiratory office.
Euvolaemia is characterised by an absence of clinical signs of dehydration, haemodynamic stability and an absenteeism of volume overload. Oliguria in this context ofttimes reflects established ATN and will not respond to increasing fluid challenges, which put the patient at risk of fluid overload. In this stage, recovery of an adequate urine output is impossible to predict. Fluid intake should exist restricted to a match daily output / losses. For patients who require ongoing maintenance IV fluids, 1 regime is to prescribe hourly crystalloid at a rate of the previous hours urine output + 30 mL.
Patients should exist carefully assessed for signs of hypervolaemia. Features may include a raised JVP, peripheral and pulmonary oedema (clinically and radiologically). Calculation of full fluid balance since admission should warning clinicians to the potential of fluid overload. In the presence of AKI, hypervolaemic patients are vulnerable to pulmonary oedema and should exist fluid restricted. There is no definitive show that the use of loop diuretics alters outcome in such patients. Nevertheless, it is advisable to consider a brusk trial of loop diuretics in patients with features suggestive of pulmonary oedema provided the patient has a reasonable perfusion pressure (MAP > 65 mmHg, SBP > 110 mmHg). Failure to reply is an indication for urgent haemodialysis and ultrafiltration.
Optimise Blood Force per unit area
Claret pressure is key to driving ultrafiltration at the glomerulus. Within the glomerulus the systemic claret pressure creates a hydrostatic pressure level of seventy mmHg. This is opposed by the colloid oncotic pressure of 30 mmHg and hydrostatic back pressure from the tubules (20 mmHg). The net filtration pressure which drives the production of up to 180 litres of glomerular filtrate is only 20 mmHg.
Absolute hypotension (defined as a SBP < 90 mmHg) has been shown to be associated with the development of AKI post-obit sepsis and major surgery16. However, relative hypotension (where in that location is a subtract in BP from pre-morbid levels in the absence of overt hypotension) has been shown to be an contained contributor to the development of AKI in elderly patients17. Maintenance of SBP according to pre- morbid values may play an of import function in preventing kidney injury in hospitalised patients.
In patients with AKI and hypotension, blood pressure level should be targeted to a MAP of > 65 mmHg. This tin can be accomplished by 3 interventions.
-
Withholding drugs that interfere with renal autoregulation (ACEi / ARBs). Temporary abeyance of all drugs that induce hypotension. This includes antihypertensives, diuretics, and agents such as nicorandil and opiates.
-
Correction of hypovolaemia as described above.
-
Consideration of vasopressor therapy (i.due east. noradrenaline) in patients refractory to acceptable correction of hypovolaemia. Vasopressors should exist considered early in such patients to avoid needless fluid overload. Patients should exist clearly identified as existence suitable for vasopressor therapy and referred to Critical Care Teams. Information technology should be stressed that in that location is no prove for a role for "renal dose" dopamine in the management of AKI. In addition, dobutamine has pregnant vasodilatory effects which can aggravate hypotension and worsen renal perfusion in patients with sepsis and AKI.
Prescribe Medicines Safely
Patients who develop AKI crave revision of all prescribed medications.
Drugs interfering with renal perfusion
These include those medications interfering with renal autoregulation (ACEi/ARBs, NSAIDs) and those medications with the potential to reduce blood pressure. Antihypertensive medications (including diuretics) should be withheld in patients with both absolute (SBP < 90 mmHg) and relative (SBP < 120 mmHg) hypotension. Patients treated with beta blockers need careful consideration of the risk / do good of temporary cessation.
Drugs requiring dose reduction or cessation
All medications that are metabolized and excreted past the kidneys should be dose adapted for an assumed eGFR of < x mL/min/i.73mii. Such drugs include fractionated heparins, opiates, penicillin-based antibiotics, sulphonylurea-based hypoglycaemic agents, and aciclovir. Although metformin is not specifically nephrotoxic, it volition accumulate in renal failure and is associated with life threatening lactic acidosis.
Drugs requiring close monitoring
These include warfarin and aminoglycosides. Gentamicin in detail demands careful consideration. Information technology should not exist withheld where there is a clear do good to its use (life threatening sepsis). If used, the daily trough level should exist < ane mg/L.
Drugs aggravating hyperkalemia
All drugs which block renal excretion of potassium (trimethoprin and potassium sparing diuretics (spironolactone, amiloride) should exist stopped. In addition, both beta-blockers and digoxin tin can inhibit the sodium / potassium ATPase pumps which move potassium within cells. The presence of these drugs can render the patient resistant to insulin/glucose treatment of hyperkalaemia.
Referral criteria to a Nephrology Team
Whilst AKI is mutual, less that 10% of such patients require direct intendance by Nephrologists2. Studies bear witness that less than 4% of hospitalized patients with AKI are treated with dialysis2.
The indication for dialysis is based on the complications of AKI rather than an absolute value for serum urea, creatinine or GFR. There is no clear benefit for undertaking dialysis solely on the footing of a low GFR. Instigation of dialysis carries with it hazard (admission issues, haemodynamic instability) and can filibuster the identification of recovery of independent renal function.
The Northern Republic of ireland GAIN guidelines18 recommend referral of the following groups of patients (Table vii).
Table 7
GAIN AKI referral guidelines.
| Referral Indication | Comments |
|---|---|
| Complications of AKI requiring dialysis | Refractory hyperkalaemia, pulmonary oedema. Severe metabolic acidosis due to kidney failure (pH < 7.2). Uraemic pericarditis and encephalopathy. |
| Suspicion of a diagnosis that may crave specialty Nephrology treatment | For example; vasculitis, myeloma, interstitial nephritis or glomerulonephritis. |
| AKI occurring in patients with CKD | Stage four or 5 CKD (eGFR ≤ 30 mL/min/1.73m2) |
| AKI occurring in renal transplant patients | Complex interactions with immunosuppressive medications. Infection can provoke acute rejection. |
Nephrology - Critical Intendance interface
Many patients develop AKI in the context of multiple organ failure. They oft manifest hypotension, severe metabolic acidosis and hypoxia due to pulmonary oedema. Such patients may require mechanical ventilation and vasopressor therapy to back up renal replacement. This level of care is all-time delivered in an Intensive Intendance Unit rather than on a Renal ward and early involvement of the Critical Intendance team should be sought.
Nephrology - Conservative care interface
It should besides be recognized that AKI may reverberate a concluding event in a hospitalised patient. Such patients usually have suffered a very severe episode of illness complicating the progression of advanced, untreatable co-morbidity.
In such patients, provision of dialysis therapy is futile, is likely to prolong suffering and lead to false hopes of survival.
Senior medical staff should place these patients early in the course of their deterioration an if necessary talk over with the Nephrology team the ceiling of intendance for renal support.
Two Scenarios
Instance 1:
A 78 year one-time adult female is admitted to the surgical ward with a left iliac fossa pain and a clinical suspicion of astute diverticulitis. She has a background of CKD (eGFR 35 mL/ min/1.73m2), hypertension treated with perindopril and type 2 diabetes treated with metformin. Ane calendar week earlier admission she developed dysuria and was empirically prescribed trimethoprim. Despite a poor oral intake during the week she continued to take all of her medication. On admission she was febrile (38oC), hypotensive (BP 80/fifty mmHg), and heart rate 120 bpm. Oxygen saturation was 96% on room air. Urine output was 5 - ten mL/hr. Investigations reveal; stage 3 AKI (creatinine 480 umol/L), hyperkalaemia - Potassium 7.1mmol/L, acidaemia (pH seven.25) with a high anion gap metabolic acidosis, elevated plasma lactate (viii mmol/L), CRP 235. She was treated with Iv Tazocin® / gentamicin and insulin/glucose for her hyperkalaemia. Over the adjacent 24 hr despite 6 L of Hartmann's solution she remained hypotensive and oliguric. Her serum creatinine rose to 650 umol/L. She became increasingly hypoxic with radiological evidence of pulmonary oedema and was transferred to ICU for mechanical ventilation, vasopressor support and dialysis. A CT scan of abdomen demonstrated a perforated sigmoid diverticulum with generalized peritonitis. She underwent a left hemicolectomy but ii days later whilst still vasopressor dependent in ICU suffered a cardiac arrest from which she did not recover.
Learning points:
Prevention: This lady was at extremely loftier risk of developing AKI in the community. She has pre-existing CKD, is elderly with significant co-morbidity and is treated with an ACEi. Such patients should be identified with from the GP register, provided with a Kidney Care Card and counseled to temporarily stop potentially nephrotoxic drugs (including metformin) during periods of poor oral intake. In add-on, trimethoprim should be used with caution in patients with Stage iv/5 CKD due to its potential to cause hyperkalaemia.
Treatment: It is essential to restore an effective blood pressure inside the starting time 4 hr of hospital admission. Failure to achieve an acceptable BP (MAP > 65 mmHg) despite an initial rapid infusion of upward to 2 Fifty of crystalloid is a marker of illness severity. In the absenteeism of obvious fluid / blood loss or cardiogenic shock, such patients should be regarded as beingness in septic shock and should be referred to the Critical Care team for consideration of vasopressor therapy. In this case additional fluids failed to restore an effective perfusion pressure level, failed to improve renal part and contributed to the evolution of pulmonary oedema. Finally this case demonstrates the high bloodshed associated with AKI where the renal insult is simply a talisman for serious underlying pathology.
Example two:
A 60 twelvemonth old man is admitted to a medical ward with a 2 week history of cough, arthralgia and reduced appetite. He had been prescribed doxycycline and a NSAID one week previously. He had a background of blazon 2 diabetes and hypertension treated with ramipril. On admission he was febrile (37.5oC), hypoxic (oxygen saturations 92% on 40% oxygen). His BP was maintained at 124/80 mmHg. His white cell count was elevated at xvi.9 and CRP was 279. His serum creatinine was 250 umol/L. An initial urinalysis was reported equally 'articulate'. Chest X-Ray showed multiple nodular opacities. Despite treatment with antibiotics, his renal office continued to deteriorate (serum creatinine 570 umol/L by twenty-four hour period iii). A repeat urinalysis demonstrated 4+ claret and 3+ protein. A subsequence vasculitis screen was positive (cANCA 120, PR3 > 8). His presentation was consistent with a diagnosis of Granulomatosis with Polyangiitis (previously known as Wegener's Granulomatosis) and he was transferred to Nephrology. He was empirically treated with pulse methyl prednisolone and Iv cyclophosphamide. A subsequent renal biopsy confirmed vasculitis. Two months after presentation his GFR was l mL/min/1.73mii and his pulmonary nodules had resolved.
Learning Points:
This patient was initially suspected to have AKI due to a combination of pneumonia and concomitant NSAID and ACEi therapy. Withal there were iii central pointers to the possibility of an intrinsic renal insult
-
The lack of a hypotensive insult during his hospital admission.
-
The presence of dipstick blood and protein.
-
The failure to meliorate despite appropriate antibody therapy targeted against pneumonia.
In patients who develop AKI evidently out of proportion to the clinical insult it is important to validate the urinalysis findings. The presence of dipstick positive blood and poly peptide should suggest a glomerulonephritis / vasculitis and an urgent renal vasculitis screen is mandated. The presence of a positive vasculitis serology in the appropriate clinical context will allow for commencement of immunosuppressive therapy prior to obtaining histological confirmation maximizing the chance of renal recovery.
Glossary
| ACEi | Angiotensin Converting Enzyme inhibitors |
| AKI | Astute Kidney Injury |
| ARB | Angiotensin Receptor Blockers |
| ATN | Astute Tubular Necrosis |
| BP | Blood Pressure |
| CKD | Chronic Kidney Disease |
| eGFR | estimated Glomerular Filtration Charge per unit |
| ESRD | Cease Phase Kidney Illness |
| Proceeds | Guidelines and Audit Implementation Network |
| GFR | Glomerular Filtration Charge per unit |
| MAP | Mean Arterial Pressure |
| NCEPOD | National Confidential Inquiry into Patient Upshot and Expiry |
| NICE | National Establish of Clinical Excellence |
| NSAIDs | Non Steroidal Antiinflamatory Drugs |
| SBP | Systolic Claret pressure level |
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Articles from The Ulster Medical Journal are provided here courtesy of Ulster Medical Society
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255835/
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