AKI and CKD Flashcards
What are the main functions of the kidneys?
The kidneys filter waste products from the blood, regulate electrolyte balance, maintain acid-base balance, regulate blood pressure, produce erythropoietin, excrete drugs, and regulate vitamin D metabolism
How does the kidney regulate blood pressure?
The kidneys regulate blood pressure through the renin-angiotensin-aldosterone system (RAAS), which helps maintain salt and water balance, ultimately influencing blood pressure.
What methods are used to measure renal function?
Renal function can be measured using serum creatinine levels, 24-hour creatinine urine collection, 51-chromium (EDTA) test, and cystatin C eGFR. Additionally, equations like MDRD eGFR, CKD-EPI formula, and Cockcroft-Gault formula are used to estimate renal function.
How is AKI defined, and why is it important?
AKI is defined as a sudden decline in renal function over hours or days, characterized by an acute rise in serum creatinine or a reduction in urine output. It’s important because it’s common, harmful, often preventable, and can lead to serious complications and even death if not managed promptly.
What are the staging criteria for AKI?
AKI is staged based on severity, with stage 1 being mild, stage 2 intermediate, and stage 3 severe. Stage 3 AKI may require renal replacement therapy such as dialysis.
What are the main causes of AKI, and how is it presented clinically?
AKI can be classified as prerenal, intrarenal, or postrenal, depending on the underlying cause. Prerenal causes include severe drop in blood pressure or interruption of blood flow, while intrarenal causes involve direct kidney damage from inflammation, toxins, or reduced blood supply. Postrenal causes result from obstruction of urine flow. Clinical presentation varies but may include nausea, vomiting, confusion, and signs of dehydration or bladder distension.
How would someone with AKI present?
- Depends on the level/cause of the AKI
- Might just be generally unwell and N+V (toxins and electrolyte build up)
- Confusion
- Palpitations (K+ increase)
- Patient might not have considered/noticed if not weeing very much
- Pre-renal cause – dehydration to shock
- Infective causes – pyrexia (increased body temp), sweating, rigors
- Post renal causes – bladder, distension, supra pubic pain
What investigations would you do for someone with AKI?
- Pharmacological - signs/Sx and review medication that may exacerbate poor renal function
- Clinical examination - Pre-renal: presents with reduced skin turgor, hypotensive, look for signs of hypovolemia
Intra-renal – rash, vasculitis lesions
Post-renal: distended bladder, stop weeing, or highly concentrated urine can show crystals upon examination
Ultrasound of renal tract or biopsy - can finds cysts, obstructions, infections, biopsy not used routinely
What are some complications of AKI
- Hyperkalemia is common, give Ca gluconate to correct, also use K+ binders
- hyperphosphatemia , reversed when kidney gets better
- hypocalcemia - only seen when prolonged AKI before medication attention due to disruption of Vit D deficiency, alfacalcidol given
- Acidosis - treated with Na carbonate
What steps do you need to take when treating AKI?
- First thing is to withhold nephrotoxic drugs
- Further treatment depends on cause/stage of AKI
- Important to keep monitoring renal function
- For some the treatment is simple e.g., if it bladder obstruction catherisation into the bladder can overcome this, we can empty the bladder and relive the pressure of the kidneys, we can then look into the cause of obscuion of bladder sepearelty
- Fluid essuction if a person is highly hypovolemic see NICE guideline for markers to use
- Fluid challenge this can be used to see if persons AKI is responsive to an increase in fluid int eh system, it is also important to do this cautiisly, give test dose and monitor to see if they can handle the small dose
- Appropriate drug dosing (frequency and strength)
- Managing patient acutely, complications and Sx
list 5 drugs to avoid or reduce in AKI?
- Statins, Opioids, NOAC, Metformin, allopurinol, bisphosphonates, ACEI/ARB, aminoglycosides (gentamycin), Lithium, NSAIDs, contrast media
What is CKD, and what are its main causes?
CKD is a condition characterized by abnormal kidney function and/or structure. Diabetes and hypertension are the main causes of CKD, but it can also result from infection, inflammation, genetic abnormalities, or structural defects.
What are the complications of CKD?
-Anaemia
- Osteodystrophy (hypocalcaemia, hyperphosphatemia, Vitamin D deficiency and hyperparathyroidism)
- Fluid retention
- Pruritus’
- Neurological problems (restless legs)
When do Sx occur and what are they?
Usually during stage 3/4 onwards, we get blood (lack of EPO production), bone (lack of Ca regulations), CVS(fluid mismanagement) and GI (increase in urea), also get peripheral neuropathy and CNS (confusion, seizure and coma) Sx
How do we reduce CVS morbidity and mortality an prevent further renal damage?
By controlling BP and proteinuria, to do this we look at albumin creatinine ratio (ACR), the higher the number the more protein has leak out of kidney (ACR marker for kidney damage). ACEI reduce proteinuria and SGLT-2I (dapagliflozin) has renal protective properties, in a diabetic where ACR>30 SGLT-2I are recommended by NICE.
