Presentation on theme: "Kidney Function & Disease NFSC 370 McCafferty. Structure Nephron: functional unit of the kidney. Each kidney has over a million nephrons. Composed of:"— Presentation transcript:
Kidney Function & Disease NFSC 370 McCafferty
Structure Nephron: functional unit of the kidney. Each kidney has over a million nephrons. Composed of: 1. Glomerulus – filtering unit –network of capillaries originating from the afferent arteriole –surrounded by Bowman’s capsule
2. Bowman’s capsule: –functions as a filter in the formation of urine 3. Tubule composed of distinct segments: –proximal tubule, descending and ascending loop of Henle, distal tubule, and collecting tubule (and collecting duct).
Glomerular Filtration: Glomerular filtrate: the fluid that filters through the glomerulus into Bowman’s Capsule, AKA glomerular capsule (pressure of blood in the glomerulus causes fluid to filter through the glomerular capillaries and into Bowman’s Capsule). From there, blood flows into the proximal tubule Loop of Henle distal tubule collecting tubule collecting duct (which collects fluid from many nephrons) Collecting duct empties into the renal pelvis ureters urinary bladder
As glomerular filtrate flows through the tubules, >99% of water and varying amounts of solutes are reabsorbed into the peritubular capillaries (capillaries that surround the tubule system). Substances are also secreted from peritubular capillaries directly into the tubular fluid to be excreted. The remaining water and solutes becomes urine.
Autoregulation of GFR: 2 Feedback Mechanisms GFR = Glomerular Filtration Rate: The volume of blood plasma filtered out of the glomeruli of both kidneys per minute. Normal GFR = ml/min Best estimate of kidney function (Note: GFR declines with age)
1.If GFR drops, afferent arteriole dilates to increase glomerular blood flow and increase pressure, thereby increasing GFR
2. If GFR drops, renin is released resulting in the conversion of angiotensin I to II. The efferent arteriole constricts, increasing glomerular pressure, and increasing GFR.
Functions of the Kidneys A. Homeostatic Functions 1. Waste excretion (urine formation) a. Nitrogenous end products: urea, creatinine, uric acid, etc. b. Metabolic degradation of peptide hormones: glucagon, insulin, PTH, growth hormone, FSH, and gastrin. 2. Fluid/electrolyte balance (Na+, K+, water) 3. Acid/base regulation: kidneys generate and reclaim filtered bicarbonate, as well as secrete excess acid to maintain balance. 4. Balance of other electrolytes (Ca++, Mg++, Phosphate PO 4 3- )
B. Non-excretory functions 1.Renin-angiotensin mechanism to control BP a.Kidney senses decreased BP b.Secretes renin (enzyme), which converts Angiotensin I to angiotensin II c.Angiotensin II is a vasoconstrictor increased BP d.Angiotensin II also stimulates aldosterone secretion e.Aldosterone increases Na+ and H 2 O reabsorption, increased plasma volume, and increased BP (aldosterone also stimulates potassium secretion into tubules)
2. Produces erythropoietin a.Stimulates erythropoiesis in bone marrow b. The anemia of CRF is primarily caused by impaired erythropoiesis c. RBC formation is mainly due to erythropoietin production in the diseased kidneys, although other compounds that accumulate in renal failure may also suppress erythropoiesis.
3. Maintains Calcium-Phosphorus bone homeostasis a.Activates Vitamin D (Hydroxylation of 25-OH-D 3 to 1,25-OH-D 3 ) in kidney disease, can supplement calcitriol, but very expensive Low vit. D less Ca++ absorbed b. Inverse relationship between Ca++ and P, so when P is retained by diseased kidney, Ca++ levels decline (less calcium reabsorbed by the kidney). c. Low serum calcium parathyroid gland releases PTH: Parathyroid Hormone: works to elevate serum Ca++ by pulling it from the bones fragility, muscular weakness, decreased muscular tone, and general neuromuscular hypoexcitability.
I.Nephritic Syndrome: group of diseases characterized by glomerular inflammation (glomerulonephritis) Hematuria, HTN, mild in renal fx. Caused by infection, SLE, other causes Acute: either resolves or nephrotic syndrome or ESRD. MNT: maintain good nutr. Status (no restriction of prot/K+) If HTN, restrict Na+ Kidney Disease
II. Nephrotic Syndrome: symptoms resulting from decreased glomerular function. Glomerular capillary permeability increases markedly (and probably capillary permeability throughout the body) Often an early sign of renal failure, especially in diabetes.
A. Characterized by: 1.Proteinuria (hallmark of nephrotic syndrome) – urinary protein loss of >3g/day (2’ increased capillary permeability) a. Hypoalbuminemia b. loss of immunoglobulins c. loss of transferrin d. loss of vitamin D binding protein
2. Edema 2’ 3. Hyperlipidemia 4. Also possible: blood coagulation disorders or increased clotting (can occlusions in lungs and legs)
B. Possible causes: 1. SLE, glomerulonephritis 2. Infections 3. diabetes mellitus 4. drugs/toxins 5. lipid nephrosis (more rare, seen in kids) lipid deposited in kidney tissue.
C. Nutrition Therapy 1.Energy: 2.High protein not recommended; accelerates kidney failure. RDA is appropriate. 3.Fat: 4.Sodium:
III. Acute Renal Failure (ARF): Sudden drop in GFR. Can develop in a previously healthy person, and last from a few days to several weeks. A. Causes 1.Prerenal: sudden drop in blood volume or renal bloodflow due to severe dehydration, shock or trauma. 2.Intrinsic: damage to kidney cells 2’ sustained shock, trauma, surgery, septicemia, nephrotoxic agents, acute glomerulonephritis. 3.Postrenal: (obstructive) Kidneys can form urine, but excretion is impeded.
B. Consequences 1.Uremic Syndrome: a.Azotemia: accumulation of nitrogenous metabolites in the blood: b.Uremia: azotemia plus the clinical signs and symptoms of weakness, ill feeling, n/v/d, itching (pruritis 2’ Ca, Na deposition), muscle cramps, hiccups, twitching, emotional irritability, mental capacity.
2. Proteinuria 3. Hyperkalemia (2’ clearance; nephropathy can cause deficiency in or resistance to aldosterone) 4. Sodium: sodium retention resulting in fluid retention, HTN, edema, CHF. –Some patients experience loss of high amounts of sodium: salt losing enteropathy. 5. Hyperphosphatemia 6. Acid-base balance: uric acid secretion and bicarbonate production metabolic acidosis
7. Blood volume changes a.Oliguric phase: very little urinary output – blood pressure rises sharply. Can pulmonary edema (remember from HTN chapter) b.Diuretic phase: large losses of fluids and electrolytes c.Recovery phase: (hopefully) – everything normalizes.
C. Treatment 1. Treat underlying disorder 2. Nutrition Therapy a.High Energy 2’ hypermetabolism – – b.Protein: depends on renal function No dialysis: Dialysis:
c. Fluid: restricted to urinary output ml for insensible losses (losses via lungs and skin). Increase if v/d/fever d. Potassium: e. Sodium: 3. Drugs a.Diuretics during oliguric phase b.Exchange resins: cause Na+ to be exchanged for K+ in the colon so K+ is excreted. c.Insulin: DM, and moves K+ into cells w/glucose
IV. Chronic Kidney Disease (CKD, previouslyCRF): Irreversible, progressive destruction of nephrons. Leads to End Stage Renal Disease (ESRD). A. Causes 1.ARF 2.Nephritis, renal artery obstruction, kidney stones, nephrotic syndrome, polycystic kidney disease 3.Diabetic nephropathy 4.HTN, atherosclerosis
B. Progression 1.Magnification Phenomenon: As GFR falls, function of remaining nephrons (adaptive hypertrophy) This is why it can go undetected. At Stage I: Protein restriction and conservative management can slow progression to ESRD. Control HTH and DM. 2.Kidney damage with normal or GFR a. renal reserve, but asymptomatic b.BUN, lytes,fluid balance, P, Ca++ ALL NORMAL
3.Renal Insufficiency a.Mild azotemia (mildly increased BUN, creat) b.Impaired concentration of urine: urine output is probably OK at this point, but because concentrating ability is impaired, we see nocturia c.Mild anemia d.Fatigue and decreased mental acuity e.Challenges will accelerate renal deterioration (ie. excessive protein load, P load, or uncontrolled HTN, DM, etc.)
4. Frank Renal Failure a.Anemia (normochromic normocytic, but low Hgb/Hct) b.Uremia c.Poss. GI ulceration and bleeding d.Skin: may become yellowed. Urea from sweat may crystallize on skin = uremic frost. Pruritis (itching) e.PEM f.HTN
g. Hypertriglyceridemia h.Hypocalcemia i.Hyperphosphatemia, poss. hyperkalemia j.Metabolic Acidosis k.Fixed urinary output l.Edema m. Altered bone metabolism - Renal osteodystrophy
5. ESRD End-Stage Renal Disease: GFR <20% of normal a.Uremia b.Kidney replacement therapy required (dialysis or transplant) c. Others: hyperchloremia, hypermagnesemia, hyperuricemia
V. Treatment of CKD Goal: delay progression of renal failure, prevent buildup of toxic metabolites, maintain or improve nutrition status, control symptoms. A. Diet (see handout)
B. Hemodialysis (HD) Method of purifying the blood in patients w/renal failure (GFR 4-5 ml/min). Takes over 2 main kidney functions: Waste removal Fluid removal
The two major forms of dialysis are hemodialysis and peritoneal dialysis. In hemodialysis, the patient’s blood is sent through a machine that filters away waste products. The clean blood is returned to the body. Hemodialysis is usually performed at a dialysis center three times per week for 3 to 4 hours.
In peritoneal dialysis, a fluid (the dialysate) is dripped into the abdomen. The dialysate captures the waste products from the blood, and after a few hours is drained away. Then, a fresh bag of dialysate is used. Patients using continuous ambulatory peritoneal dialysis (CAPD), the most common form of peritoneal dialysis, change dialysate four times a day. Another form of peritoneal dialysis, however, can be performed at night with a machine that drains and refills the abdomen automatically. Patients can perform peritoneal dialysis themselves.
VI. Consequences of CKD Osteodystrophies: 1. P retention leads to serum Ca++ with PTH secretion. Results in Ca++ being removed from bones. Also in renal failure: intestinal absorption of Ca++ 2.Tendency toward spontaneous fractures, painful joints, bone pain, metastatc calcification. Cardiovascular Disease 1.Atherosclerosis: accelerated in CRF. TG, esp w/HD 2.HTN due to Na+ and fluid retention, as well as alteration in renin-angiotensin mechanism 3.Pericarditis: etiology unknown
Hematologic abnormalities: : 1.Anemia is almost universal 2.EPO, Fe Cardiovascular Disease GI disorders: Loss of appetite, n/v, may also see changes in GI motility and absorption; GI hemorrhage Neuropathy: 1.CNS manifestations:” fatigue, insomnia, depression, agitation; also convulsions, coma, and death 2.“dialysis dementia,” related to aluminum