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Renal Diseases
Remedios Adamos- Magkasi, MD, MHPEd, FPSP, FPSMID

Normal Kidney (please refer on separate sheet)

Renal Artery

Anterior branch

Posterior Branch

Interlobar Artery

Arcuate Arteries

Interlobular Arteries Afferent arterioles Glomerulus

Efferent arteriole
TUBULES 1. PROXIMAL CONVOLUTED TUBULE (PCT) ✔ Abundant long microvilli, which forms a brush border that partly obscures the lumen and increases surface area available for absorption. ✔ Increased Mitochondria, required for the energy-intensive abdorptive function interdigitate with basal membrane infoldings and make the lining cells acidophilic ✔ Apical Canaliculi ✔ Increased intercellular digitations ✔ Reabsorbs glucose, amino acids, vitamins, proteins, acetoacetate, 2/3 of water, 2/3 of sodium

1. JUXTAGLOMERULAR APPARATUS (refer on separate sheet)

in particular. FILTER PLASMA – modify filtrate – urine a.dihydroxycholecalciferol a. Urea. ✔ Permeable to both water and salt. 1.hydroxylase is synthesized in the proximal renal tubule cells ✔ Converts 25-hydroxycholecaliferol to 1. PRODUCE HORMONES a. ✔ These symporter thes increases the salt concentration (and tonicity. Control Fluid and electrolyte balance c. ✔ Impermeable to water. or osmolarity) in the interstitium.25. Blood Vessels) Reason: 1. Second hydroxylation of Vitamin D ✔ 1-alpha.25 – DIHYDROXY VITAMIN D ✔ Increases gastrointestinal reabsorption of calcium and phosphorus ✔ Promotes bone mineralization. creatinine. MAINTAINS CALCIUM HOMEOSTASIS a. Contribute to Acid-Base Balance ✔ Controls the synthesis and excretion of bicarbonate and hydrogen ions 1. ✔ Contains NA+/K+/Cl. Useful in Diagnosis ✔ The kidneys have a large functional reserve and manifest when much damage has occurred . although it is more permeable to water. DISTAL COLLECTING TUBULES ✔ Acidification of urine (H+) PHYSIOLOGY (refer on separate sheet) FUNCTIONS OF THE RENAL SYSTEM 1. uric acid b. 1. ✔ Loses water. LOOP OF HENLE LOOP OF HENLE FUNCTION: A prerequisite for forming hypertonic urine. ASCENDING AND DESCENDING LIMB. may reabsorb some salt from interstitium ASCENDING PART ✔ More active role in setting up the gradient and.pump (symporter) that constantly pums these ions (in a 1:1:2 ratio) from the filtrate into the interstitial fluid around the tubules. RENIN – regulates vascular tone – increase in blood pressure b.2. maintains serum calcium PATHOLOGY OF RENAL DISEASES Traditional approach: BASIS – morphologic renal components (Glomerulus. tubules. the loop acts as a countercurrent multiplier to establish an osmotic gradient in the interstitial fluid of the medulla. Interstitium. ERYTHROPOIETIN – synthesized in the renal cortex by interstitial cells in the peritubular capillary bed 1. Excretes waste material Ex. Water in the filtrate cannot follow the salt into the interstitium and dilute it. making the medullary interstitium hypertonic. DESCENDING PART ✔ Plays a passive role in making the medullary interstitium hypertonic and helps maintain the gradient.

Glomerulus – Immune Injury Tubules. HsC) ✔ Treponema ✔ Falciparum ✔ Malaria a. Exogenous ✔ Bacterial products ✔ Viral antigen (HsB. All forms of chronic diseases will destroy all 4 components – End-Stage Chronic Renal Failure GLOMERULAR DISEASES GENERAL PATHOGENESIS: Immune Mechanisms 1. damage to one almost always affect the others 1. Endogenous – auto . parasitic. Some components are more vulnerable to specific forms of injury Ex. interstitium – toxic. drugs Antigen + Antibody Antigen – Antibody complex + Granular deposits ( by immunofluorescence stain) 1. Heyman Nephritis – Granular Immunofluorescence C. Anti-GBM Nephritis – Linear Immunofluorescence B. IN-SITU/ CIRCULATING ANTIBODY – MEDIATED A. infectious 2. Antibody against planted Antigen Ex.✔ Early signs and symptoms are important ✔ Later. CIRCULATING IMMUNE COMPLEX (IC) NEPHRITIS trapped in glomeruli a. bacterial. Viral.

Anti-GBM Ab – initiate / facilitate glomerular injury by activated T cells = Exper. CYTOTOXIC Ab ✔ Mesangial Cells – Lysis ✔ Endothelial Cells – injury – thrombosis ✔ Epithelial Cells – injury – Proteinuria (leakage) 1.Localization a. CRESCENTERIC GN 2. Neutral – in mesangium Immune Complex digested Subside (limited exposure) Re-exposed .show of Ag (SLE. GN 1. ALTERNATE – C PATHWAY ACTIVATION ✔ MEMBRANO-PROLIFERATIVE GN TYPE II (Dense deposit disease) Ab + Ag (epithelial cell) ✔ Effaced foot processes ✔ Vacuolation detaches from PROTEINURIA MEDIATORS OF GLOMERULAR INJURY (ACUTE/ CHRONIC INFLAMMATION) 1. Large – removed by MPS b. CMI – sensitized T-Lymphocytes Ex. CELLS a. Anionic – do not cross GBM – subendothelial d. PMN. viral hepatitis) Cycles of IC deposits Chronic membranous GN Chronic mem-prolif. Cationic – croos GBM – subepithelial c. monocytes .

Coagulation system OUTCOME OF RENAL DISEASES DISEASE Decreased GFR (30 to 50% of Progress (constant rate) END-STAGE KIDNEY FAILURE (regardless of stimulus) DIALYSIS TRANSPLANTATIO NN SECONDARY FACTORS LEADING TO PROGRESSION 1. Glomerular/ Mesangial Cells 1. Cytokines c. T-lyphocytes. permeability . Eicosanoids. FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS) 2.b. Chemokines d. Complement b. endothelin e. Prevented or delayed HISTOLOGIC CHARACTRISTICS OF RENAL DAMAGE 1. Macrophages. NK cells c. Soluble Mediators a. TUBULO-INTERSTITIAL FIBROSIS a. FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS) Diseased Kid Affected Unaffected Endothelial injury Epithelial Injury (podocytes) Inc. No angiotensin. Platelets d.