Renal failure develops when there is a reduction in the kidneys’ ability to sufficiently filter waste products from the blood. It is caused by a wide variety of diseases and medications with acute or chronic effects on renal vasculature, the tubules, or the glomerulus.
Acute Kidney Injury
Acute kidney injury (AKI), formerly called acute kidney failure, is a sudden decline in glomerular filtration rate (GFR). This results in elevations in serum creatinine (SCr), blood urea nitrogen (BUN) and electrolyte levels (Okusa and Rosner, 2019). Acute kidney injury is a clinical spectrum: it may be rapidly reversible with prompt identification and treatment of the underlying cause, such as fluids for dehydration, or removal of a nephrotoxin. Conversely there may be life-threatening fluid overload or electrolyte disturbances requiring emergent dialysis before the cause has even been established. Many cases of AKI occur in patients hospitalized for unrelated acute illness.
Chronic Kidney Disease
Chronic kidney disease (CKD) is defined as the presence of kidney damage or decreased GFR for greater than 3 months. Kidney damage is characterized by albuminuria, urine casts, imaging findings, or abnormal renal biopsy. CKD is caused by long term diseases such as diabetes or hypertension. Patients can present with symptoms resulting directly from diminished kidney function. These include malaise, nausea, decreased mental acuity, edema or decreased urine output. However, many patients have no clinical symptoms. In such patients, kidney disease is detected by laboratory tests that are obtained through routine screening or as part of an evaluation of an unrelated illness. The stages of CKD are a continuum and are
classified as follows (Kellum and Lemeire, 2012):
- Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)
- Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)
- Stage 3a: Moderate reduction in GFR (45-59 mL/min/1.73 m2)
- Stage 3b: Moderate reduction in GFR (30-44 mL/min/1.73 m2)
- Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)
- Stage 5: Kidney failure (GFR < 15 mL/min/1.73 m2 or dialysis)
The table below outlines the clinical features of AKI and CKD. However, it is somewhat misleading to present AKI and CKD as completely distinct clinical entities. In recent years CKD has been recognized as a major risk factor for the development of new AKI, and patients with CKD who develop AKI often recover incompletely and experience accelerated renal deterioration (Ferenbach and Bonventure, 2016).
* KDIGO Clinical Practice Guideline for Acute Kidney Injury
|Clinical Features of Acute Kidney Injury and Chronic Kidney Disease
||Acute Kidney Injury
||Chronic Kidney Disease
||Gradual (months to years)
- Acute tubular necrosis (ischemia or nephrotoxin exposure)
- Pre-renal disease (hypovolemic states, hypotension)
- Urinary tract obstruction (prostate disease, metastatic cancer)
- Diabetic nephropathy
- Polycystic kidney disease
- Nephrotoxin exposure
||One of the following:
- Increase in serum creatinine (SCr) by 0.3 mg/dl within 48 hours
- Increase in SCr to 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days
- Urine volume < 0.5 ml/kg/hr over 6 hours (Kellum and Lemeire, 2012)
|One of the following, for at least 3 months:
- Kidney damage (albuminuria, urine casts, abnormal renal biopsy or imaging)
- Decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least 3 months (Kellum and Lemeire, 2012)
- Low or no urine volume, hematuria, edema, confusion, shortness of breath
- Symptoms are often associated with the cause (thirst in patients with dehydration, flank pain in patients with obstruction)
- Many patients have no symptoms
- Weakness, fatigue, anorexia, edema, nausea/vomiting, decreased urine output
- Many patients are asymptomatic until CKD is advanced
- Identify the etiology
- Treat reversible causes, such as hypotension, volume depletion, or urinary tract obstruction
- Remove any nephrotoxic medications to minimize new injury
- Identify and treat the complications such as fluid overload, hyperkalemia, and acidemia
- Optimally manage the underlying disease process
- Remove any nephrotoxic medications
- Monitor and correct water and electrolyte imbalance
- Regulation of blood pressure to low-normal values
- Treat renal anemia and osteopathy
To summarize, AKI develops suddenly from an acute renal insult and encompasses a spectrum of renal impairment from minor changes in markers of renal function to requirement for renal replacement therapy (RRT). The management of AKI involves identifying and treating the underlying case as well as minimizing complications. AKI is usually reversible. In contrast, CKD develops gradually, over months to years, as a result of chronic illnesses such as diabetes and hypertension. Patients are often asymptomatic and CKD is discovered incidentally on routine screening or workup of unrelated diseases. Medical treatment may slow the progress of renal failure but it is irreversible and eventually leads to the need for kidney transplant or permanent dialysis.
Ferenbach, D. A. and Bonventre, J. V. (2016, April). Acute kidney injury and chronic kidney disease: from the laboratory to the clinic. Nephrologie & Therapeutique, 12(suppl 1): S41-S48.
Kellum, J. A. and Lameire, N. (2012, March). KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements, Volume 2, supplement 1.
Levey, A. S. and Inker, L. A. (2018). Definition and staging of chronic kidney disease in adults. UpToDate. Retrieved from https://www.uptodate.com/contents/definition-and-staging-of-chronic-kidney-disease-in-adults
Okusa, M. D., and Rosner, M. H. (2019). Overview of the management of acute kidney injury (AKI) in adults. UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-the-management-of-acute-kidney-injury-aki-in-adults
Tomino, Y. (2014). Pathogenesis and treatment of chronic kidney disease: a review of our recent basic and clinical data. Kidney and Blood Pressure Research, 39:450-489.