Acute Kidney Injury
Clinical Presentation and Causes of AKI
Lyz Boyd
Learning Objectives
By the end of this chapter, you will be able to:
- Identify common blood test values which determine kidney function.
- Explain common signs and symptoms of AKI based on pre-, intra-, and postrenal causes
General Presentation
As you might imagine, the clinical presentation of AKI can differ depending on the cause. However, the basic criteria for AKI apply to all causes which include:
- An increase in serum creatinine OR
- An abnormally small volume of urine production
Let’s briefly learn about what creatinine is and how it relates to the function of the kidneys. Creatinine is a waste molecule produced by muscle tissue that is excreted by the kidneys. It is produced at a relatively constant rate every day, and therefore excreted in the same way. A sudden rise in creatinine in the blood can be indicative of AKI because it reflects the fact that the kidneys are not excreting it properly into the urine. Seeing as creatinine levels are related to muscle mass, everyone’s normal level is different depending on factors like sex, age, and weight. Therefore, it’s best when healthcare providers have a previous value to compare to, but that is not always available.
Both an increase in serum creatinine or a decrease in urine production indicate that the kidneys are not working normally and an AKI is present.
Key Takeaways
- Nephrons are damaged and can no longer control urine formation, leading to changes in volume of urination (little or no urine production) AND excess fluid in tissues (edema)
- Nephrons are damaged and can no longer control reabsorption of useful substrates nor eliminate waste. This causes a rise in nitrogenous wastes in blood (since it can’t be excreted)
Regardless of the cause, if AKI is not corrected it will progress, resulting in a build up of toxic waste products in the body, along with other disruptions to the delicate balances of the body, such as pH balance and electrolyte concentrations. Build up of waste products like urea may progress to a condition called uremic encephalopathy, where the function of the brain becomes impacted by these toxins. Symptoms of uremic encephalopathy include confusion, seizures, and coma.
Specific Presentations
The following table summarizes the specific presentations of different causes of AKI, in addition to increase in blood creatinine levels and low urine output:
| Cause of AKI | Description of Pathology | Clinical presentation |
| Prerenal causes | ||
| Acute hemorrhage (hypovolemic/hemorrhagic shock) | Decreased blood pressure due to blood loss and therefore decreased blood volume | Low blood pressure, tachycardia, tachypnea, reduced level of consciousness, evidence of hemorrhage (may be internal or external) |
| Gastrointestinal fluid losses (hypovolemic shock) | Decreased blood pressure due to fluid losses | Low blood pressure, tachycardia, tachypnea, recent or current vomiting/diarrhea |
| Acute congestive heart failure exacerbation (cardiogenic shock) | Decreased heart function due to heart pathology (eg: cardiomyopathy, muscle damage from a past ischemic event) such that the heart can no longer maintain adequate blood flow to the body | Electrocardiogram (ECG) abnormalities, low blood pressure, tachycardia, shortness of breath, enlarged heart. Pulmonary edema (fluid build up) from fluid backup into lungs, may hear crackles with a stethoscope. Peripheral edema from fluid build-up in the periphery (usually the lower legs). |
| Sepsis (septic shock) | Systemic inflammatory response to an infection, often a bloodstream infection. Inability to maintain adequate blood pressure due to dilation of blood vessels all over the body (vasodilation). | Fever, warm extremities (from vasodilation), low blood pressure, tachycardia, history or signs of an infectious source (eg: skin wound, pneumonia) |
| Massive pulmonary embolism (obstructive shock) | Obstruction of the pulmonary (lung) blood vessels (usually by a blood clot) that increases pressure in the right side of the heart and reduces blood returning to the left side of the heart to a degree that impairs blood flow to the body. | Low blood pressure, tachycardia, shortness of breath, chest pain, cough, hemoptysis (coughing up blood). |
| Intrarenal causes | ||
| Acute tubular necrosis | Damage to renal tubule cells from ischemia (lack of blood flow) or toxin. Examples of toxins include medications or toxin release from another pathological process, such as rhabdomyolysis (muscle breakdown, myoglobin release) or hemolytic uremic syndrome (E. coli toxin from intestinal infection). | History of prolonged renal ischemia, history of medication known to cause ATN, muscle tenderness (rhabdomyolysis), or history of gastrointestinal illness. |
| Glomerulonephritis | Various causes are possible, but all are encompassed by immune-mediated damage to components of the renal corpuscle. | Hematuria (blood in the urine), proteinuria (protein in the urine), highly elevated blood pressure which may further cause confusion or headache, edema (usually in the periphery or around the eyes) |
| Acute interstitial nephritis | A type of allergic reaction to a drug or pathogen that affects the interstitium of the kidneys. | Variable, can be asymptomatic or may have nausea, vomiting, and/or flank pain. Skin rash and a fever are also possible. |
| Postrenal causes | ||
| Benign prostatic hyperplasia | The prostate gland (present in biological males) located around the urethra near the bladder outlet, gradually enlarges over time. If the obstruction of the urethra becomes severe enough, it can entirely block urination and cause AKI by urine backing up into the urinary system. | History of lower urinary tract symptoms which include weak stream, straining to urinate, hesitancy (difficulty initiating urination), nocturia (frequent waking at night to urinate), frequency (needing to urinate many times during the day), and urgency (sensation of an urgent need to urinate). Abdominal or flank pain |
| Tumour | Tumours of the urinary system, abdomen, or reproductive system can compress structures involved in urine transport which may result in AKI. | non-specific symptoms that affect the whole body and are often associated with cancer or infection – such as unintentional weight loss, fever, excessive sweating at night, and fatigue. In the case of prostate carcinoma, metastasis to the bone is common, so bone pain or back pain is possible. |
| Kidney stone | Stones that form in the kidneys may become suddenly stuck in a ureter, causing obstruction and impaired kidney function if the other kidney is unable to compensate or if stones are present on both sides. | Flank pain with radiation to the groin. |
Critical Thinking Exercises
Answer these questions for yourself
Section Summary
Manifestations of AKI are varied due to the underlying cause of the kidney injury. Because nephrons are damaged and can no longer control blood filtration and urine formation, renal manifestations would be changes in volume of urination (little or no urine production), excess fluid in tissues (edema), rise of nitrogenous wastes in the blood (e.g. high serum creatinine). These manifestations are in addition to those seen with the original cause. Manifestations of pre-renal causes will have signs of poor blood flow and/or low blood volume (e.g. low blood pressure). Intrarenal causes could have signs of inflammation (e.g. fever). Post-renal causes would have difficulty with urination and possible pain at the location of the obstruction.
