Chronic Pyelonephritis PDF

# Chronic Pyelonephritis - Disorder in which chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis - Pelvicalyceal damage an important diagnostic characteristic - Reflux is an important cause of kidney destruction in children with lower UTI # Clinical Features - grad...

# Chronic Pyelonephritis - Disorder in which chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis - Pelvicalyceal damage an important diagnostic characteristic - Reflux is an important cause of kidney destruction in children with lower UTI # Clinical Features - gradual onset of renal insufficiency and hypertension - polyuria and nocturia due to loss of concentrating ability due to tubular dysfunction - asymmetrically contracted kidneys with characteristic coarse scars and blunting and deformity of the calyceal system - Significant bacteriuria in early stages and absent in late stages - Secondary FSGS common several years after scarring - onset of proteinuria poor prognostic sign and progression to ESRD increased # Toxin Induced Tubulointerstitial Nephritis - Toxins are second most common cause 1. trigger an interstitial immunologic reaction, exemplified by the acute hypersensitivity nephritis induced by drugs such as methicillin 2. cause ATI, as described earlier 3. cause subclinical but cumulative injury to tubules that takes years to result in chronic kidney disease may be unrecognized and progress to irreversible renal damage # Acid-Base Disorders | Acid-Base Disorder | Effect on pH | Primary Change | Compensation | |---|---|---|---| | **ACIDOSIS** | | | | | Metabolic Acidosis | ↓pH | ↓HCO3- | ↓PCO2 | | Respiratory Acidosis | ↓pH | ↑PCO2 | ↑HCO3- | | **ALKALOSIS** | | | | | Metabolic Alkalosis | ↑pH | ↑HCO3- | ↑PCO2 | | Respiratory Alkalosis | ↑pH | ↓PCO2 | ↑HCO3- | # Acidosis and alkalosis A flowchart describing acidosis and alkalosis. # Alkalosis A flowchart describing alkalosis. # Met. Alkalosis Formula - Normal values: pH= 7.40, HCO3-= 24, PaCO2= 40 - If Met. Alk - Ur < 20 -> non-renal (chloride responsive) - Ex. Vomiting, Recent diuretics taken - Ur > 20 -> renal (Cl- resistant, direct excretion)-> 1 Cl- out -> 1 HCO3- in - Bartter (loop), Gietelman (thiazide), increased BP (hyperaldosternosim), current diuretics - Winter's Formula for correction - PaCO2= 0.7(HCO3¯ - 24) + 42 = ANS ± 2 # Met. Acidosis Formula - AG= [Na+] - ([Cl-]+[HCO3-])= ANS ± 2 - Use ALWAYS - Corrected AG = [Na+] - [Cl-] - [HCO3-] + 2.5(4 - Albumin) = ANS - Use if asked for - UrAG = [UrNa+] + [UrK+] - [UrCl-]= ANS ±2 - Use urine values - Use in NAGMA - If UAG (+)-> Renal Causes - If UAG (-)-> Non-renal causes (Cl- lost= NH4+ lost -> kidneys are working) - Winter's Correction formula - PaCO2= 1.5(HCO3-)+10= ANS ± 2 - NAGMA-> HARDASS - HAGMA-> GOLDMARK # Diuretics # Diagram of diuretic moa A diagram showing the mechanism of action of different types of diuretics including: mannitol, acetazolamide, loop diuretics, thiazide diuretics and potassium sparing diuretics. | MoA | Site | Targets | indications | adv effects | |---|---|---|---|---| | Osmotic | - | - | - | - | | Mannitol | - | - | | | - | Glomerulus | - | - | | | - | PCT | - | - | | | - | Descending Loop of Henle | - | - | | | - | - | ↓ICP (cerebral edema) | - | | | - | - | ↓intraocular pressure (glaucoma) | - | | | - | - | Initiating hemodialysis | - | | | - | - | ↓chemo side effects | - | | | - | - | Drug overdose (induces toxin elimination) | - | | | - | - | Inhaled for CF | - | | | - | - | Extracellular vol expansion worsens HF & pulmonary edema | - | | | - | - | Dehydration | - | | | - | - | Hyperkalemia | - | | | - | - | Hypernatremia | - | | | - | - | Acute renal failure | - | | | - | - | ↑ urine NaCl | - | | Carbonic Anhydrase Inhibitors | - | - | - | - | | Acetazolamide | Carbonic Anhydrase 1-4,7,12, 14 antagonist <br> AQP 1 antagonist | Proximal tubule <br> Thick ascending Loop of Henle <br> Late DCT | - | - | | | - | - | CSF leak | - | | | - | - |Glaucoma | - | | | - | - | Epilepsy | - | | | - | - | Hyperphosphatemia | - | | | - | - | Acute Mountain sickness | - | | | - | - | Metabolic alkalosis | - | | | - | - | Urine alkalinization | - | | | - | - | - | - | | | - | - | Hyperchloremic Metabolic Acidosis (type 2 RTA) | - | | | - | - | Renal stones (Ca+P04-) | - | | | - | - | Renal K wasting (hypokalemia) | - | | | - | - | Drowsiness | - | | | - | - | Paresthesia | - | | | - | - | "Acid azolamide causes acidosis" | - | | | - | - | ↑ urine NaCl | - | | | - | - | ↑NaHCO3 | - | | Loop diuretics | - | - | - | - | | Furosemide | SLC12A1 or NKCC2 <br> Carbonic Anhydrase 2 inhibitor <br> G-protein receptor 35 agonist | Thick ascending Loop of Henle <br> Proximal tubule <br> Distal tubule | - | - | | | - | - | Edema (HF, pulmonary edema, cirrhosis, Nephrotic Syndrome) | - | | | - | - | HYTN (hypertension) | - | | | - | - | Acute Renal failure | - | | | - | - | HyperCalcemia | - | | | - | - | Anion overdose intoxication (Br, F, I) | - | | | - | - | Ototoxicity | - | | | - | - | Hypokalemia | - | | | - | - | Hypomagnesemia | - | | | - | - | Dehydration | - | | | - | - | sulfa Allergy | - | | | - | - | metabolic Alkalosis | - | | | - | - | Nephritis | - | | | - | - | Gout | - | | | - | - | ↑ urine NaCl | - | | | - | - | ↑ urine K | - | | | - | - | ↑urine Ca | - | | | - | - | "Loop earrings hurt your ears" | - | | | - | - | - | - | | | - | - | "Loops lose Ca+" | - | | | - | - | - | - | | Thiazides | - | - | - | - | | hydrochlorothiazide | SLC12A3 or NCC (NaCl co) <br> Ca-activated K channel subunit a1 | Early DCT | - | - | | | - | - | HYTN (w ACEi or ARB) | - | | | - | - | HF (edema) | - | | | - | - | Nephrolithiasis due to Idiopathic Hypercalciuria | - | | | - | - | Nephrogenic Diabetes Insipidus | - | | | - | - | HOTN | - | | | - | - | Hypokalemic Metabolic alkalosis | - | | | - | - | Hyponatremia | - | | | - | - | - | - | | | - | - | - | - | | | - | - | "HyperGLUC" | - | | | - | - | HyperGlycemia | - | | | - | - | HyperLipidemia | - | | | - | - | HyperUricemia | - | | | - | - | HyperCalcemia | - | | | - | - | ↑ urine NaCl | - | | | - | - | ↑ urine K | - | | | - | - | ↓ urine Ca | - | | | - | - | - | - | | K-sparing diuretics | - | - | - | - | | Spironolactone, Eplerenone, A | - | DCT | - | - | | | - | - | - | - | | | - | - | - | - | | | - | - | 1ry & 2ry hyperaldosteronism | - | | | - | - | Fibrotic/inflammatory aldosterone | - | | | - | - | HYTN | - | | | - | - | MI | - | | | - | - | Liddle syndrome | - | | | - | - | Hepatic ascites | - | | | - | - | Antiandrogen | - | | | - | - | Hyperkalemias (high w renin inhibibitors) | - | | | - | - | Hyperchloremic metabolic acidosis type IV Renal Tubular acidosis | - | | | - | - | Gynecomastia (spironolactone) | - | | | - | - | Acute Renal failure (triamterene/indomethacin) | - | | | - | - | Kidney stones (triamterene) | - | | | - | - | ↑ urine NaCl | - | | | - | - | ↓ urine K | - | | | - | - | - | - | | | - | - | - | - | | | - | - | - | - | # Diagram showing sites of actions of diuretics A diagram showing the sites of action of different types of diuretics. # Diuretics: electrolyte changes - **Urine NaCl** - ↑ with all diuretics (concentration varies based on potency of diuretic effect). Serum NaCl may decrease as a result. - **Urine K** - ↑ especially with loop and thiazide diuretics, excluding K-sparing diuretics. - **Blood pH** - ↓ (acidemia): carbonic anhydrase inhibitors: + HCO, reabsorption. K sparing: aldosterone blockade prevents K secretion and H secretion. Additionally, hyperkalemia leads to K entering all cells (via H/K exchanger) in exchange for H exiting cells. - ↑ (alkalemia): loop diuretics and thiazides cause alkalemia through several mechanisms: - · Volume contraction→AT II Na/H exchange in PCTHCO, reabsorption ("contraction alkalosis") - · Kloss leads to K' exiting all cells (via H/K exchanger) in exchange for H entering cells - · In low K state, H' (rather than K') is exchanged for Na' in cortical collecting tubule → alkalosis and "paradoxical aciduria" - **Urine Ca2+** - ↑ with loop diuretics: paracellular Ca¹ reabsorption hypocalcemia. - + with thiazides: enhanced Cat reabsorption. # Nephrotic Syndrome # Nephrotic syndrome - Proteinuria more or equal 3.5 (Nephrotic range) - Hypoalbuminemia → decrease oncotic pressure → edema - Hypercoagulable state by loss of AT II - Hyperlipidemia/Hypercholesterolemia → Fatty cast # Minimal Change - More commonly in childrens after a URT infection, Immunization or Atopic disorders (Idiopathic). - Associated with Hodking Lymphoma - Massive cytokines release (IL-13) cause loss of podocytes. - Selective albuminuria - Respond to steroids (vs FSGS) - Normal glomeruli, IF negative but EM with podocyte effacement # Focal Segmental Glomerulos Sclerosis - Hispanic, African American Adults. - Idiopathic, HIV, Heroin or Sickle Cell. - H&E: Focal segmental collagen deposition (pink) - EM: effacement of foot process - IF: Non specific - Resistant to steroids (vs MC) - Can progress to renal failure. # Membranous Nephropathy - Caucasian - Idiopathic, SLE, Hepatitis B&C, Solid tumors, NSAIDS or Penincillamines - No Hypercellular (vs Membranous Proliferative) - Thick glomerular BM (Membranous) - Granular IF by immune complex deposition - SubEpithelial deposit → SPIKES AND DOMES # Membranous Proliferative Nephropathy - Thick capillaries membrane and mesangial proliferation with tram-tracks. - Granular IF with SubEndothelial deposition. - Nephritic or Neprotic - 2 Types: - Type 1: Under endothelial cells by Hepatitis B&C. - Tram-track associated by new BM synthesis - Type 2: In BM by C3 Nephritic Factor that stabilize C3 convertase # Diabetic Nephropathy - Hyaline arteriosclerosis - Afect efferent arteriole more - Microalbuminuria and eGFR - Sclerosis of mesangium - Nephrotic Kimmelstiel-Wilson Nodules - ACE inhibitors # Systemic Amyloidosis - Deposit in mesangium - Proliferation - By chronic inflammation (tuberculosis) or Multiple myeloma - Congo red stain with apple freen briefinger under light. # Images of Diabetic Nephropathy and Systemic Amyloidosis Two pictures comparing diabetic nephropathy and systemic amyloidosis under a microscope.