Urgent considerations
Your Organizational Guidance
ebpracticenet urges you to prioritize the following organizational guidance:
Chronisch nierlijden (multidisciplinaire aanpak)Published by: WORELLast published: 2017GPC pluridisciplinaire sur la néphropathie chronique (IRC)Published by: Groupe de travail Développement de recommandations de première ligneLast published: 2017See Differentials for more details
Multiple cholesterol emboli syndrome
Multiple cholesterol emboli syndrome (MCES) is characterized by elevated serum creatinine days or weeks following arterial manipulation, vascular surgery, stent placement, or cardiac catheterization. It is a stepwise, acute or subacute, progressive rise in serum creatinine, and includes multiorgan involvement (cutaneous lesions, "thrash toes, blue toes," pancreatitis, stroke, ischemic bowel, angina). A high index of suspicion is required for diagnosis.[70] Prompt evaluation and supportive medical management is recommended.[71]
MCES should be distinguished from contrast-induced acute kidney injury, where multiorgan involvement is absent, and serum creatinine rises within 48 hours, peaks, then returns to baseline within 7 to 10 days.
Contrast-induced acute kidney injury
Contrast-induced acute kidney injury (CI-AKI) (formerly known as contrast-induced nephropathy) is a sudden deterioration in renal function caused by the administration of iodinated contrast medium. Criteria for diagnosis vary; an increase in baseline serum creatinine concentration of at least 0.3 mg/dL within 48 hours after exposure to contrast media is often used.[72] CI-AKI usually peaks at 4 to 5 days and returns to baseline within 7 to 10 days.
Pre-existing renal insufficiency is the most significant risk factor.[72] Treatment is supportive. Differential diagnosis includes MCES.
Prophylaxis with intravenous normal saline is indicated for patients without contraindication who have AKI or an eGFR less than 30 mL/minute/1.73 m² who are not undergoing maintenance dialysis.[73]
Pregnancy-related elevations in creatinine
Normal serum creatinine during pregnancy is 0.4 to 0.5 mg/dL (36 to 45 mmol/L), and values above this are of concern. A rise in serum creatinine may imply pregnancy-related acute kidney injury or the progression of undetected or known CKD. During pregnancy, a woman may lose up to 50% of her renal function and still maintain serum creatinine <1.5 mg/dL because of hyperfiltration in the remaining nephrons.[74]
Renal blood flow and glomerular filtration rate are decreased in preeclampsia, and an increase in serum creatinine may be seen in the later stages. Prompt evaluation to exclude these causes is required in all patients.
Renal transplant rejection
Most acute renal transplant rejections occur in the first 3 months. Serum creatinine elevation is usually the alerting event for the clinician, and may be associated with fever, oliguria, and graft tenderness. Other reasons for elevated serum creatinine include surgical and infection complications, immunosuppressive medications, and noncompliance with medications. Elevated serum creatinine in a transplant recipient requires prompt evaluation by an organ transplant specialist.
Traumatic renal infarction
Traumatic renal infarction occurs in 1% to 2% of all nonpenetrating abdominal trauma. Likelihood is increased in the presence of lumbar vertebral injury.[67] A high index of suspicion is required for diagnosis.
Initial screening tests may include computed tomography (CT) abdomen and pelvis with contrast and angiography. The rate of successful revascularization is low, even with early detection. Prompt evaluation is required.
Renal vein thrombosis
Loin, testicular, or flank pain in patients with solitary kidney, renal transplant, systemic lupus erythematosus, or nephrotic syndrome may be the presenting symptom of renal vein thrombosis and can be associated with hematuria, increased proteinuria, and elevated serum creatinine.
Renal Doppler ultrasound and magnetic resonance venography are useful imaging tools.[75] Prompt admission to the hospital and initiation of anticoagulant therapy are usually required.
Rapidly progressive glomerulonephritis
Renal vasculitis may present as rapidly progressive glomerulonephritis with acute kidney injury, proteinuria and hematuria. ANCA-associated vasculitis is the most common cause in the elderly population.
Rapidly progressing glomerulonephritis may be a uremic emergency requiring prompt initiation of supportive care and dialysis support. Patients require urgent nephrology consultation for consideration of renal biopsy. Specific therapies include plasma exchange and immunosuppression.[76]
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End-stage renal disease patient with uremic symptoms
People with noncompliant or poorly maintained end-stage renal disease undergoing dialysis may present with uremic signs and symptoms, including pericarditis and pericardial effusion. Prompt and rigorous dialysis therapy may treat pericarditis and prevent cardiac tamponade.
Sepsis
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.[77] Up to 60% of patients with sepsis have acute kidney injury (AKI). The deleterious inflammatory cascade characteristic of sepsis, hypovolemia, and/or exposure to nephrotoxic therapies contribute to the AKI.
Patients with sepsis complicated by AKI have a significantly increased mortality relative to patients without AKI. Patients with AKI associated with sepsis have a significantly increased mortality relative to those with AKI of another etiology.[78]
Presentation ranges from subtle, nonspecific symptoms (e.g., feeling unwell with a normal temperature) to severe symptoms with evidence of multiorgan dysfunction and septic shock. Patients may have signs of tachycardia, tachypnea, hypotension, fever or hypothermia, poor capillary refill, mottled or ashen skin, cyanosis, newly altered mental state or reduced urine output.[79] Sepsis and septic shock are medical emergencies.
Risk factors for sepsis include: age under 1 year, age over 75 years, frailty, impaired immunity (due to illness or drugs), recent surgery or other invasive procedures, any breach of skin integrity (e.g., cuts, burns), intravenous drug misuse, indwelling lines or catheters, and pregnancy or recent pregnancy.[79]
Early recognition of sepsis is essential because early treatment improves outcomes.[79][80][Evidence C][Evidence C] However, detection can be challenging because the clinical presentation of sepsis can be subtle and nonspecific. A low threshold for suspecting sepsis is therefore important. The key to early recognition is the systematic identification of any patient who has signs or symptoms suggestive of infection and is at risk of deterioration due to organ dysfunction. Several risk stratification approaches have been proposed. All rely on a structured clinical assessment and recording of the patient’s vital signs.[79][81][82][83][84] It is important to check local guidance for information on which approach your institution recommends. The timeline of ensuing investigations and treatment should be guided by this early assessment.[83]
Treatment guidelines have been produced by the Surviving Sepsis Campaign and remain the most widely accepted standards.[80][85] Recommended treatment of patients with suspected sepsis is:
Measure lactate level, and remeasure lactate if initial lactate is elevated (>2 mmol/L).
Obtain blood cultures before administering antibiotics.
Administer broad-spectrum antibiotics (with methicillin-resistant Staphylococcus aureus [MRSA] coverage if there is high risk of MRSA) for adults with possible septic shock or a high likelihood for sepsis.
For adults with sepsis or septic shock at high risk of fungal infection, empiric antifungal therapy should be administered.
Begin rapid administration of crystalloid fluids for hypotension or lactate level ≥4 mmol/L. Consult local protocols.
Administer vasopressors peripherally if hypotensive during or after fluid resuscitation to maintain MAP ≥65 mmHg, rather than delaying initiation until a central venous access is secured. Norepinephrine (noradrenaline) is the vasopressor of choice.
For adults with sepsis-induced hypoxemic respiratory failure, high flow nasal oxygen should be given.
Ideally these interventions should all begin in the first hour after sepsis recognition.[85]
For adults with possible sepsis without shock, if concern for infection persists, antibiotics should be given within 3 hours from the time when sepsis was first recognized.[80] For adults with a low likelihood of infection and without shock, antibiotics can be deferred while continuing to closely monitor the patient.[80]
Giving excess fluids to patients with AKI is harmful. Over-resuscitation and under-resuscitation have both been associated with adverse outcomes in the setting of shock.[78]
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