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30 Cards in this Set
- Front
- Back
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effect Angiotensin II (ATII)
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Vasoconstricts peripheral resistance arterioles and efferent arterioles
Stimulates the synthesis and release of aldosterone |
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effect Renal-derived prostaglandin (PGE2)
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Vasodilates the afferent arterioles
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where is Produces erythropoietin
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Synthesized in the endothelial cells in the peritubular capillaries. Erythropoiesis is the production of RBCs in the bone marrow and is dependent on the release of erythropoietin from the kidneys.
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where Second hydroxylation of vitamin D
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1-α-Hydroxylase is synthesized in the proximal renal tubule cells.
Converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol. |
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Functions of vitamin D
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Increases gastrointestinal reabsorption of calcium and phosphorus
Promotes bone mineralization by stimulating the release of alkaline phosphatase from osteoblasts. Alkaline phosphatase hydrolyzes pyrophosphate and other inhibitors of calcium-phosphate crystallization. Increases the production of osteoclasts from macrophage stem cells |
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Upper urinary tract (kidneys, ureter) causes of hematuria
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Renal stone
Glomerulonephritis Characterized by dysmorphic RBCs (irregular membrane) Renal cell carcinoma |
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Lower urinary tract (bladder, urethra, prostate) causes of hematuria
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Infection
Transitional cell carcinoma Most common cause of gross hematuria in the absence of infection Benign prostatic hyperplasia Most common cause of microscopic hematuria in adult males |
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Drugs associated with hematuria
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Anticoagulants (warfarin, heparin)
Cyclophosphamide Hemorrhagic cystitis Risk factor for transitional cell carcinoma |
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Types of Proteinuria Functional
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Protein <2g/24 hours
Not associated with renal disease |
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Types of Proteinuria
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Protein loss is variable
Low-molecular-weight proteinuria Amount filtered >tubular reabsorption |
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Types of Proteinuria Glomerular
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Nephritic syndrome: protein >150 mg/24 hours but <3.5g/24 hours
Nephrotic syndrome: protein >3.5g/24 hours |
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Types of Proteinuria
Tubular |
Protein <2g/24 hours
Defect in proximal tubule reabsorption of low-molecular-weight proteins (e.g., amino acids) at normal filtered loads |
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serum BUN
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Normal serum BUN 7 to 18 mg/dL
End product of amino acid and pyrimidine metabolism Produced by the liver urea cycle Filtered in the kidneys Partly reabsorbed in the proximal tubule Serum levels depend on the following: Glomerular filtration rate (GFR) Protein content in the diet Proximal tubule reabsorption Functional status of the urea cycle |
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creatinine, urea - kidney processes?
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Creatinine is filtered and is neither reabsorbed nor secreted.
Urea is filtered and partly reabsorbed in the proximal tubule |
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define azotemia?
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Azotemia refers to an increase in serum BUN and creatinine.
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prerenal azotemia
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Caused by a decrease in cardiac output
Hypoperfusion of the kidneys decreases GFR. There is no intrinsic renal parenchymal disease. Examples-blood loss, congestive heart failure Serum BUN:Cr ratio greater than 15 Decreased GFR causes creatinine and urea to back up in blood. After filtration, some urea is reabsorbed back into the blood. All of the creatinine is excreted in the urine. Addition of urea to blood increases the ratio to over 15. Example-serum BUN 80 mg/dL, serum creatinine 4 mg/dL BUN/Cr ratio is 20. |
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renal azotemia (uremia)
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Caused by parenchymal damage to the kidneys
Examples-acute tubular necrosis, chronic renal failure Serum BUN:Cr ratio is 15 or below. Decreased GFR causes creatinine and urea to back up in blood. After filtration, both urea and creatinine are lost in the urine. Proximal tubule cells are sloughed off in renal failure. Serum BUN:Cr ratio is maintained (i.e., ≤15) Example-serum BUN 80 mg/dL, serum creatinine 8 mg/dL BUN/Cr ratio is 10. |
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Postrenal azotemia
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Caused by urinary tract obstruction below the kidneys
No intrinsic parenchymal disease Examples-prostate hyperplasia, blockage of ureters by stones/cancer Serum BUN:Cr ratio greater than 15 Obstruction to urine flow decreases the GFR Back-up of urea and creatinine in the blood Increased tubular pressure causes back-diffusion of urea (not creatinine) into blood (ratio >15). Persistent obstruction causes renal azotemia (ratio ≤ 15). |
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Is all elevated BUN ARF?
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Steroids
Increased catabolic rate Febrile, bed-bound, septic ICU patients Tetracycline antibiotics Parenteral nutrition Gastrointestinal Bleeding |
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Is all elevated creatinine ARF?
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Factitious ARF
Interference with laboratory measurement of Scr (Jaffe Method) creatinine+picric acid in alkaline solution results in the formation of a red compound used to measure creatinine Cefoxitin Ketoacids Competitive inhibition of creatinine secretion in the proximal tubule Cimetidine trimethoprim Increased production of creatinine fenofibrate |
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prerenal azotemia causes?
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1. Decreased intravascular volume
Hemorrhage Renal losses Osmotic diuresis “GUM” Diabetes Insipidis Salt wasting nephritis GI losses Vomiting and diarrhea Insensible losses 3rd spacing Burns Pancreatitis Peritonitis Ileus 2. Decreased cardiac output AMI (cardiogenic shock) CHF PE Cardiac Tamponade 3. Peripheral vasodilatation BP meds Gram-negative shock Anaphylactic reactions Hepato-renal Syndrome 4. Increased renal vascular resistance Anesthesia Fluid shifts intraoperatively Prostaglandin inhibitors (NSAIDS) Vasoconstriction Calcineurin inhibitors (cyclosporine) Radiocontrast dye 5. Decreased intraglomerular pressure 6. ACE/AT II inhibition |
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DIALYSIS indications
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Acidosis
Electrolytes (K+) Intoxicants (LISA MET BARB) Overload Uremia LIthium SAlicylates Methanol Ethylene glycol Theophylline BARBituates |
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ethylene glycol ingestion sxs? tx?
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drunkenness, coma, tachypnea, pulmonary edema, flank pain, renal failure. urine examine wood's light (UV). tx alcohol or fomepizole + dialysis
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FeNa <1%
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not unique to Pre-renal Azotemia
Renal Artery Stenosis Acute Glomerulonephritis Non-oliguric ATN, especially early contrast-induced nephropathy ATN when Pigment Nephropathy Contrast Nephropathy Early urinary tract obstruction |
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FeNa >1%
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FeNa > 1% does not mean the patient isn’t Pre-renal
Elderly patients CKD patients Diuretic use Poor nutritional intake Intrinsic Vascular Large vessel Renal Artery Stenosis Embolism Atheroembolic disease Endocarditis Thrombus Vasculitis Small vessel Vasculitis Atheroembolic disease Microangiopathic HUS/TTP Malignant Hypertension Pregancy-related HELLP |
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Intrinsic: Tubular
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Acute Tubular Necrosis or ATN
Ischemic (50%) Biliary surgery Gram-negative sepsis Hemorrhage Trauma Nephrotoxic (35%) Contrast Induced Nephropathy Aminoglycosides Amphotericin B Tumor Lysis Syndrome Ethylene Glycol Poisoning Cisplatin Pigment Hemoglobin (hemolysis) Myoglobin (rhabdomyolysis) |
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Intrinsic: Vascular
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Type I: Anti-GBM
Goodpastures (IF has Linear deposition pattern) Type II: Immune-complex (IF has Granular deposition pattern) Post-streptococcal GN Lupus Nephritis IgA Nephropathy Henoch-Schönlein Purpura Membranoproliferative GN Type III: (IF has Pauci-immune deposition pattern) Wegener’s Granulomatosis Microscopic Polyangiitis Idiopathic crescentic Rales, JVD, HTN, edema, oliguria; Serologic work-up: Anti-GBM Ab, P-ANCA, C-ANCA, dsDNA, ANA, C3C4, ASO, anti-DNAse B Specific gravity may be elevated, RBC casts and dysmorphic RBC’s; urine Na may be low, FeNa < 1% Type I: Cytoxan + steroids + plasmapheresis; Type II and III: Cytoxan + steroids |
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Intrinsic: Glomerular
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RPGN
Hematuria, dysmorphic RBC’s, RBC casts Oliguria Edema. Hypertension Interstitial Acute Interstitial Nephritis |
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Intrinsic: Interstitial
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Drug hypersensitivity (70%)
30% Antibiotics: PCNs (Methicillin), Cephalosporins, Quinolones NSAIDs Sulfa drugs (Bactrim, Lasix, Bumex) Allopurinol Proton Pump Inhibitors Infection (15%) Strep, Legionella, CMV, other bact/viruses Autoimmune (6%) Sarcoid Sjogrens Tubulointerstitial nephritis withUveitis (TINU) Idiopathic (8%) 3-5 d to develop AIN after second exposure to drug . May take wks after initial exposure to drug. Up to 18 months to get AIN from NSAIDS. Rash — 15% , Fever — 27%, Eosinophilia — 23% , Triad of rash, fever, and eosinophilia — 10% Bland sediment or WBCs, RBCs, non-nephrotic proteinuria. WBC Casts. Normal or only mildly increased protein excretion (less than 1 g/day). Urine eosinophils on Wright’s or Hansel’s Stain. Also see urine eos in RPGN, renal atheroemboli, acute prostatitis, and occasionally, acute cystitis. Gallium scan (positive gallium scan is suggestive of AIN in the presence of the above characteristic findings but a negative scan does not preclude the diagnosis, since false negative results can be seen). diffuse, intense, bilateral uptake, consistent with the interstitial inflammatory infiltrate |
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Post-renal Failure (Obstructive)
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Ureteral
Stones Clots Pyogenic debris Edema from a retrograde pyelogram Bladder neck BPH Drugs Autonomic Neuropathy Bladder Cancer Ganglionic Blocking Agents Urethral Valves Strictures Extrinsic Compression Extrinsic compression from tumor Retroperitoneal fibrosis Cervical Cancer Accidental ureteral ligation Intra-abdominal Compartment Syndrome |
