How does the body maintain fluid balance?
-Kidneys produce renin which interacts w/ renin-angiotensin-aldosterone-system (RAAS) to regulate fluid balance
-Input + production = utilization + output
-Vasopressin opens channels in kidney letting water follow NaCl into bloodstream which promotes reabsorption
-Atrial Natriuretic Factor (ANF) causes Na + H2O to be excreted via urine when fluid volume is too high
-Hormones influence permeability of nephrons controlling mvmt of Na & Cl back out into blood
-K+ secreted from bloodstream –> nephron –> urine
Describe what happens at different sections of the nephron
-Nephron: Functional unit of the kidney, filters ~48 gal. of blood daily & helps maintain homeostasis
-Renal corpuscle: Composed of the glomerulus & Bowman’s capsule; it’s the primary blood filtering unit
-Proximal convoluted tubule: Reabsorbs AAs, Na, bicarb, K, Ca & H2O; also secretes drugs and produces ammonium
-Loop of Henle: Concentrates urine and regulates fluid sent to collecting ducts & ureters
-Distal tubule: Reabsorbs 99% of filtrate into vasa recta and includes thick ascending limb which is regulated by vasopressin, PTH & calcitonin; macula densa senses Na & releases renin; maintains electrolyte balance
-Collecting duct: Principal cells reabsorb NaCl & secrete K+ and intercalated cells regulate acid-base balance by secreting H+ & bicarb
Describe how the body registers changes in fluid balance within the cardiovasculature and responds hormonally
-ADH: Enhances water reabsorption by increasing Na channels in kidney principal cells
-Angiotensin II: Stimulates ADH secretion, promoting H2O retention
-ANP: Decreases ADH secretion, helping regulate blood volume & pressure
-When responding to hemorrhage, BV reduction leads to lower mean arterial pressure (MAP)
-ADH & RAAS are activated to facilitate H2O retention and vasoconstriction to stabilize cardiovascular function
Describe the interaction of the specific hormones’ actions at the nephron including the medullary osmotic gradient
-Medullary osmotic gradient: Decreases osmolarity near cortex & increases near renal pelvis; also facilitates water reabsorption via osmosis
Water reabsorption breakdown:
-70% in the proximal tubule (passive, unregulated)
-20% in distal tubule (regulated by ADH)
-10% in the collecting ducts (influenced by ADH)
Role of ADH:
-Stimulates aquaporin-2 channels in distal tubule & collecting ducts; they increase H2O permeability, enhancing reabsorption into bloodstream
-ADH adjusts H2O permeability in distal tubules/collecting ducts while medullary osmotic gradient ensures H2O conservation & fluid balance
Describe the difference between how the respiratory system compensates for acidosis vs. how the renal system compensates
-Acidosis can result from increased CO2 (respiratory) or excess H+ (metabolic); blood pH < 7.35
-Respiratory system enhances ventilation rate, allowing more CO2 to be exhaled; this decreases CO2 in blood & helps to raise the pH
-Renal system excretes more H+ into urine & reabsorbs/synthesizes more bicarb to further buffer blood & restore pH balance
-Respiratory has quick response (within minutes-hours) & renal has slower response (hours-days)
How does hypertension cause kidney disease?
-HTN damages blood vessels (including those in kidneys) and causes vessel walls to thicken & narrow –> decreased blood supply
-Decreased blood supply impairs kidneys’ ability to filter waste & leads to buildup of waste/fluids in the body
-Uncontrolled HTN can lead to kidney failure, requiring dialysis/transplant
-Chronic high BP can worsen pre-existing kidney damage, accelerating decline in function
How does diabetes cause kidney disease?
-Diabetic nephropathy: Gradual loss of kidney function in people w/ DM caused by prolonged exposure to high BG which impairs waste filtration
-Early sign is glomerular hyperfiltration where excessive blood filtering strains nephrons
-Glomeruli become leaky forming advanced glycation end products (AGEs), which causes inflammation & scarring leading to impaired nephron function
-High BP (common in DM) worsens kidney damage
How is CKD classified?
Classification based on glomerular filtration rate (GFR), which measures how well kidneys are functioning
What is happening at CKD Stage 1?
-There’s kidney damage but GFR remains normal/increased (> 90 mL/min)
-Damage is minimal & often only detected through protein in urine or physical damage seen on imaging
What is happening at CKD Stage 2?
-Damage progresses, GFR mildly decreased (60-89 mL/min)
-Kidneys still function enough to prevent waste buildup
-Early detection at this stage is CRUCIAL for managing & slowing the progression of this disease
What is happening at CKD Stage 3?
-Stage 3a: Moderate decrease in GFR (45-59 mL/min) & Stage 3b: GFR of 30-44 mL/min
-Function continues to decrease & kidneys may no longer adequately filter waste leading to toxin buildup
-Symptoms include fatigue, fluid retention, changes in urination & discomfort in kidney area
-CKD often detected at this stage
What is happening at CKD Stage 4?
-Severe decrease in GFR (15-29 mL/min)
-Kidneys no longer filtering waste leading to more pronounced symptoms like anemia, decreased appetite, bone disease & abnormal levels of phos, K+ & other lytes
-Risk of CVD significantly increases
What is happening at CKD Stage 5?
-AKA kidney failure or ESRD
-GFR < 15 mL/min, kidneys lost almost all ability to function, significant buildup of waste products/lyte imbalances/fluid overload
-Dialysis or transplant needed for survival
-Symptoms include N/V, breathlessness, confusion & loss of appetite
Explain why people with CKD may get osteoporosis?
-Disruptions in Ca & bone metabolism
-PTH acts on both kidneys & bones by influencing synthesis of the active form of vitamin D (1,25-dihydroxycholecalciferol)
-As kidney function decreases, kidneys become less able to excrete phosphate & activate vitamin D which leads to elevated phos levels & decreased Ca absorption (both which stimulate parathyroid gland to release more PTH)
-When PTH above normal range, patients are at risk for secondary hyperparathyroidism which leads to increased Ca serum levels, excessive bone resorption & potential tissue calcification
-When GFR is <30 mL/min, kidneys lose ability to convert vitamin D in active form and places a greater burden on bones to release Ca leading to bones being broken down worsening risk of osteoporosis
Explain why patients with CKD often become anemic
-Erythropoietin (EPO) production is decreased and is a hormone that stimulates bone marrow to produce RBCs
-In CKD, decreased RBC production & shortened lifespan lead to anemia
-CKD can also lead to an iron deficiency because it interferes w/ body’s ability to absorb & use iron, which is essential for RBC production (iron loss in urine, decreased intake due to restrictions & inflammation associated)
-Dialysis also plays a role due to blood loss during and the use of heparin
What is a pre-renal AKI?
-When there’s an obstruction of blood flow to kidneys
-Results from decreased cardiac output, hypovolemia, vascular emboli, HF & LF or meds that affect blood supply
-Can be reversed within couple days when normal blood flow is restored
-But if underlying cause is not effectively treated, could lead to intra-renal
What is a intra-renal AKI?
-Involves damage to kidney cells themselves
-Can be caused by nephrotoxic agents, infections, or systemic diseases (lupus or sarcoidosis)
-Sepsis from pre-renal can trigger intra-renal
-More severe and likely alters nutritional requirements of the patient, where they will need careful monitoring & management
What is a post-renal AKI?
-Obstruction in flow of urine from kidneys
-From kidney stones, enlarged prostate, cervical cancer or other tumors
-Can often be reversed within a few days once the obstruction is cleared
-No change in nutrition but very important to focus on addressing obstruction to restore function
Explain why someone might want to ensure at least some nutrition is flowing through the gut, even if someone is receiving parenteral nutrition
-Preserves gut health by maintaining GI barrier function & mucosal integrity; also supports digestion & nutrient absorption
-Prevents infections by strengthening mucosal barrier, reducing bacterial translocation (bacteria/toxins entering bloodstream)
-Boosts immunity by enhancing systemic & local immune responses; stimulates epithelial cell metabolism, turnover & intestinal blood flow
-Promotes release of trophic hormones essential for gut health
-Supports gut tissue by preventing atrophy of Gut-Associated Lymphoid Tissue (GALT) & Mucosa-Associated Lymphoid Tissue (MALT)
-Combats malnutrition by addressing complications from impaired nutrient absorption & supports immune system function
What is at risk if we don’t confirm enteral tube placement before we begin tube feeding?
-Tube can mistakenly go down the trachea into the lungs, EN could end up filling the lungs
-Can lead to aspiration pneumonia, where food/liquid enters the lungs rather than stomach and can cause infections & death
-Important to check placement through CT scan
In more highly concentrated enteral formulas, why is there a higher percentage of calories from fat?
-Fat is the most calorie-dense macronutrient and allows a significant amount of energy to be delivered in a smaller volume, especially for patients w/ fluid restrictions
-As formula concentration increases, the osmolarity of formula also increases
-By increasing %kcals from fat, the formula can deliver more kcals without exacerbating osmolarity-related issues
Describe refeeding syndrome
-Series of metabolic & electrolyte disturbances that can occur when calories are reintroduced or increased after a period of significantly decreased or absent calorie intake
-Hallmarks include hypophosphatemia, hypokalemia & hypomagnesemia
-Can develop with reintroduction of kcals from any source shifting metabolism from fat to carb metabolism increasing insulin production and decreasing glucagon production
-Increased insulin production drives phos, K+, and Mg into cells, depleting already low reserves which exacerbates risk of dangerous imbalances
Why does refeeding syndrome happen?
-During malnutrition, body relies on glycogenolysis (glycogen breakdown) & gluconeogenesis (glucose creation) for energy
-Liver glycogen depletes in 12-24 hours, shifting to ketones from fat oxidation
-Intracellular depletion of phos, K+ & Mg occurs to maintain balance
-Serum levels appear normal, masking growing intracellular deficits
-Insulin secretion increases with feeding, driving glucose & lytes (especially phos) into cells
-Rapid carb metabolism depletes Mg & thiamin
-Thiamin stores are naturally low with a half-life of 7-10 days, deficiency can lead to refeeding syndrome
How is refeeding syndrome prevented?
-Involves starting caloric intake slowly & gradually increasing over several days
-Do this by monitoring and supplementing lytes & thiamin prior to and during refeeding
-Also regularly assess lab values & patient symptoms to address imbalances early