Quiz 2 Flashcards
Major indications for dialysis?
ARF, CRF (creatinine clearance < 8ml/min), anuria
What are the 2 major forms of dialysis?
Peritoneal (intracorporeal) and hemodialysis and hemofiltration (extracorporal).
What do both of the 2 major forms of dialysis do?
Replace function of glomeruli with a semi-permeable membrane.
Do you generally use peritoneal dialysis or hemodialysis first?
Generally peritoneal before hemodialysis.
What are the 3 types of peritoneal dialysis?
- CAPD (continuous ambulatory peritoneal dialysis)
- CCPD (continuous cyclic peritoneal dialysis)
- IPD (intermittent peritoneal dialysis)
Benefits of peritoneal dialysis over hemodialysis?
- Greatly reduced protein losses
- Much better control of K+ and phosphorous levels
- Rarely need water and sodium restriction because 2 L per d removed in the peritoneal fluid
Causes of structural changes in diabetic nephropathy?
- Glycosylation of proteins damage GBM (thickening)
- Hemodynamic changes –> glomerular hypertrophy (sclerosis)
Result of structural changes dt diabetic nephropathy?
Structural and functional changes to GBM dt hyperglycemia –> inc GBM collagen type IV, inc fibronectin, inc reactive oxidative species, increased circulating AGEs (normally excreted in urine)
How to monitor diabetic nephropathy?
- Microalbumin (random am sample or 24 hr collection)
- HbA1c levels (measuring glycated hemoglobin—average level of glucose an RBC has been exposed to in its 120 day life-cycle)
Microalbumin normal and abnormal ranges?
Normal: 0-30 mg/dL
Microalbuminuria: 30 - 300 mg/dL
Macroalbuminuria: >300 mg/dL
Target lab values for diabetes management?
- A1C ≤6.5%
- FPG <110 mg/dl
- Blood pressure < 130/80mmHg
- Lipids: LDL <100, HDL: >40 mg/dl men, >50 mg/dl women, TG: <150 mg/dl
Definition of hypertensive nephropathy and nephrosclerosis? Major cause?
Narrowing of the arteries that carry blood to the kidney. MC cause is atherosclerosis.
Hypertensive nephropathy/nephrosclerosis pathogenesis?
Reduced blood flow causes affected kidney(s) to secrete renin, retain NaCl and H2O⇒inc BP Hypersecretion of renin also caused by sodium depletion, hemorrhage, shock, CHF, renal artery stenosis
Treatment and management of hypertensive nephropathy/nephrosclerosis?
- Control BP with meds: diuretics, beta-blockers, Ca channel blockers, ACEis, ARBs. (ACEIs most effective in both managing HTN and slower progression of renal disease in African Americans)
- Percutaneous transluminal angioplasty (insertion of a stent)
- Surgical reconstruction of damaged artery
- Surgical bypass of renal arteries in cases of fibromuscular hyperplasia
- Treat atherosclerosis: guggal, garlic, EFAs, B vits
- Vascular protectants: bioflavonoids, vaccinium
What is nephroptosis?
- Kidney drops >5cm upon moving from supine to standing position.
- Theorized to be due to lack of perirenal fat and fascial support. Also pts have longer than normal renal vascular pedicle.
- More common in females 5-10:1, young and thin, more common on right side.
- 64% of those with fibromuscular dysplasia of renal artery have nephroptosis.
S/sxs of nephroptosis:
Severe abdominal, costovertebral, flank pain and vomiting when moving into upright position.
What is a Dietl crisis and why does it occur?
Dietl Crisis: severe colicky flank pain, nausea, vomiting, chills, tachycardia, oliguria, hematuria and proteinuria. Occurs d/t nephroptosis.
What are renal cysts?
Epithelium-lined cavities filled with fluid or semi-solid material, developing from tubular elements.
Tell me all about simple or solitary cysts.
- 65-70% of all renal masses usu found incidentally, often located in outer cortex and contain fluid consistent with an ultrafiltrate of plasma.
- Usu asymptomatic, but may become infected, or if large may block ureter and cause hydronephrosis.
- Average size: 10cm.
Autosomal Dominant Polycystic Kidney Disease (ADPKD)?
- Most common hereditary dz in US.
- Bilaterally enlarged kidneys with multiple cysts of various sizes.
- 1:400-1000 persons, 6000 new cases/yr.
- Symptoms appear >40 yo.
- 50% may also have hepatic, pancreatic, splenic or CNS arachnoid cysts.
- Most patients have normal kidney function until 4th decade.
Cystogenic process of ADPKD?
- Mutation in renal tubule cell causes cellular division until cysts develop.
- As cysts enlarge, they destroy anatomy and cause progressive functional impairment, may get infected, bleed, etc.
Dx of ADPKD?
- 15-39 yo: at least 3 cysts in both kidneys
- 40-59 yo: at least 2 cysts
- AND (for all): positive FHx
S/sxs of ADPKD?
- Pain over both kidneys due to infection, obstruction, hemorrhage, “drag” from heaviness.
- Gross hematuria HTN (retinopathy)
- Nocturia
- Palpable, nodular kidney
- Renal insufficiency: HA, N+V, weight loss
- If infected: fever, chills, tender kidney(s)
Labs in ADPKD?
- Inc erythropoietin, leading to inc HGB and HCT
- Anemia from blood loss
- Proteinuria, hematuria, possibly pyuria and bacteriuria
- Progressive uremia from renal insufficiency (BUN and creatinine)
Imaging in ADPKD?
- KUB—enlarged renal shadows up to 5X size
- CT—95% accurate for dx, can detect cysts from 0.5cm
- US—can detect cysts from 1-1.5cm (Most cost effective, usu start here)
- MRI can differentiate Renal Cell Carcinoma (RCC) from cysts
ADPKD naturopathic tx?
- Low protein diet - 0.5-0.75 g/kg/d
- Force fluids to 3000 ml or more per day (to suppress plasma vasopressin)
- Restrict caffeine
- Flax oil
- Reasonable physical activity - avoid strenuous activity or contact sports
- Treat uremia, stones, infection when present
- Screen for and treat HTN. Recommended ACE inhibitors, Angiotensin II receptor antagonist blockers
- Poss tx: dialysis, renal transplantation, cystic decompression (for pain)
- Constitutional HP: tumors, cystic—Baryta carb, Calc carb, Phos
- Constitutional hydro
- Conventional drug trials: somatostatin, everolimus (mTOR inhibitor)
MC type of benign renal tumor?
Renal Adenoma.
Most common. Small, well-differentiated glandular tumors of renal cortex. Asymptomatic and usually identified at autopsy. Some can metastasize.
Adenocarcinoma or Renal Cell Carcinoma (RCC or RCA) risk factors?
- Cigarette smoking
- Chronic analgesic use
- ADPKD
- Obesity
- Toxin exposure (Cd, Pb, asbestos, PAHs)
- Coffee
- Animal fat diet
- Dialysis, hysterectomy, contrast IVU, Von Hippel-Landau dz
RCC pathogenesis?
- RCC originates from the proximal renal tubular epithelium in the cortex. Tumor is nodular, distorted, bulges the shape of the kidney.
S/sxs of RCC?
- “Great masquerader”
- Classic triad: gross hematuria, flank pain, palpable abd mass
- Fever, weight loss, HTN
- In males: possible L varicocele from blockage of L testicular vein
- Sx of metastasis: dyspnea, cough (lung), seizure (brain), bone pain
How does RCC spread?
- Direct invasion through the renal capsule into adjacent structures, or;
- Direct extension into the renal vein.
Where does RCC most commonly metastasize to?
- Metastasizes via lymph and blood vessels, most commonly the lung
- Also bone, regional nodes, adrenal gland, brain, opposite kidney, adjacent organs, subcutaneous tissue.
- 25-30% of patients have metastatic disease at presentation.
Nephroblastoma (Wilms’ Tumor) definition?
- A mixed malignant tumor of the kidney which is seen more often in children than adults, median 3.5 yrs.
- Abnormal proliferation of metanephric blastema cells, genetic predisposition.
Ssx of nephroblastoma?
Presents as abdominal mass, abd pain, hypertension, hematuria, anemia.
