Anatomy and Physiology of UrinarySystem WIDODO BAGIAN ANESTESIOLOGI, PERAWATAN INTENSIF, DAN PENANGANAN NYERI RSUP WAHIDIN SUDIROHUSODO MAKASSAR Introduction Organ system that produces, stores, and carries urine Humans produce about 1.5 liters of urine over 24 hours, although this amount may vary according to the circumstances. Increased fluid intake generally increases urine production. Increased perspiration and respiration may decrease the amount of fluid excreted through the kidneys. Some medications interfere directly or indirectly with urine production, such as diuretics. Components of system –Kidneys –Ureters –Bladder –Urethra Kidney Location and External Anatomy toxins) Production and secretion of hormones Regulation of blood pressure .Functions of the Kidney: Maintaining balance Regulation of body fluid volume and osmolality Regulation of electrolyte balance Regulation of acid-base balance Excretion of waste products (urea. drugs. ammonia. Renal Artery C. Renal Vein B. Medulla E. Ureter D. Proximal tubule 5. Renal Pelvis F.The Kidney and the Nephron A. Cortex 1. Distal tubule . Ascending loop of Henle 2. Peritubular capillaries 4. Descending loop of Henle 3. Glomerulus 6. 000) Responsible for urine formation: – – – Filtration Secretion Reabsorption .000.The Nephron Functional unit of the kidney (1. Components of the nephron •Glomerulus •Afferent and Efferent arterioles •Proximal Tubule •Loop of Henle •Distal Tubule •Collecting Duct . Overview of nephron function From http://www.emc.edu/faculty/farabee/BIOBK/BioBookEXCRET.html .maricopa. Filtration . THE GLOMERULUS . Plasma is filtered through the glomerular barrier •Components of plasma cross the three layers of the glomerular barrier during filtration •Capillary endothelium •Basement membrane (net negative charge) •Epithelium of Bowman’s Capsule (Podocytes –filtration slits allow size <60kD) •The ability of a molecule to cross the membrane depends on size.it is NOT URINE YET! . charge. and shape • Glomerular filtrate therefore contains all molecules not contained by the glomerular barrier . 2 L/h=180 L/day!! (99% of fluid filtered is reabs.Glomerular Filtration Rate (GFR) Measure of functional capacity of the kidney Dependent on difference in pressures between capillaries and Bowman’s space Normal = 120 ml/min =7.) . The Response to a Reduction in the GFR . Reabsorption and secretion . . etc) – Na+ antiporters (H+) – Ion channels – Osmosis . a. K+ ATP pumps Passive Transport– Na+ symporters (glucose.a.Reabsorption Active Transport –requires ATP – Na+. Factors influencing Reabsorption Saturation: Transporters can get saturated by high concentrations of a substance failure to resorb all of it results in its loss in the urine (eg. . Rate of flow of the filtrate: affects the time available for the transporters to reabsorb molecules. renal threshold for glucose is about 180mg/dl). Distal tubule . Ca2+. and small proteins are also reabsorbed here.reabsorbs the remaining 2% of Na+ only if the hormone aldosterone is present. . 75-90% of H20. Loop of Henle .reabsorbs 65 % of filtered Na+ as well as Cl-. H20 depending on hormone ADH. Collecting duct . Reabsorbs HCO3-.reabsorbs 25% of filtered Na+. carbohydrates. HCO3-.What is Reabsorbed Where? Proximal tubule . Glucose. amino acids. PO4.reabsorbs 8% of filtered Na+. . Secretion Proximal tubule – uric acid. . drugs. some drugs. K+. some creatinine Distal tubule – Most active secretion takes place here including organic acids. bile salts. H+. TammHorsfall protein (main component of hyaline casts). metabolites. Image from http://en.Countercurrent exchange The structure and transport properties of the loop of Henle in the nephron create the Countercurrent multiplier effect. A substance to be exchanged moves across a permeable barrier in the direction from greater to lesser concentration.wikipedia.org/wiki/Countercurrent_exchange . H20 Ascending loop is impermeable to H20. Cl-.Loop of Henle – Goal= make isotonic filtrate into hypertonic urine (don’t waste H20!!) – Counter-current multiplier: Descending loop is permeable to Na+.active NaCl transport Creates concentration gradient in interstitium Urine actually leaves hypotonic but CD takes adv in making hypertonic . Vitamin D3: – Enzyme converts Vit D to active form 1.25(OH)2VitD. which in turn ultimately leads to retention of salt and water. Involved in calcium homeostasis. Erythropoietin: – Stimulates red blood cell development in bone marrow. Renin leads to production of angiotensin II.Hormones Produced by the Kidney Renin: – Released from juxtaglomerular apparatus when low blood flow or low Na+. Will increase when blood oxygen low and anemia (low hemoglobin). . Renin, Angiotensin, Aldosterone: Regulation of Salt/Water Balance Aldosterone Secreted by the adrenal glands in response to angiotensin II or high potassium Acts in distal nephron to increase resorption of Na+ and Cl- and the secretion of K+ and H+ NaCl resorption causes passive retention of H2O Anti-Diuretic Hormone (ADH) Osmoreceptors in the brain (hypothalamus) sense Na+ concentration of blood. High Na+ (blood is highly concentrated) stimulates posterior pituitary to secrete ADH. ADH upregulates water channels on the collecting ducts of the nephrons in the kidneys. This leads to increased water resorption and decrease in Na concentration by dilution Ureters Slender tubes that convey urine from the kidneys to the bladder Ureters enter the base of the bladder through the posterior wall – This closes their distal ends as bladder pressure increases and prevents backflow of urine into the ureters Ureters Ureters have a trilayered wall – Transitional epithelial mucosa – Smooth muscle muscularis – Fibrous connective tissue adventitia Ureters actively propel urine to the bladder via response to smooth muscle stretch . collapsible. muscular sac that temporarily stores urine It lies retroperitoneally on the pelvic floor posterior to the pubic symphysis – Males – prostate gland surrounds the neck inferiorly – Females – anterior to the vagina and uterus Trigone – triangular area outlined by the openings for the ureters and the urethra – Clinically important because infections tend to persist in this region Chapter 25: Urinary System 29 .Urinary Bladder Smooth. Urinary Bladder The bladder wall has three layers – Transitional epithelial mucosa – A thick muscular layer – A fibrous adventitia The bladder is distensible and collapses when empty As urine accumulates. the bladder expands without significant rise in internal pressure Chapter 25: Urinary System 30 . Urinary Bladder Chapter 25: Urinary System 3125.18a. b Figure . Urethra Muscular tube that: – Drains urine from the bladder – Conveys it out of the body . Urethra Sphincters keep the urethra closed when urine is not being passed – Internal urethral sphincter – involuntary sphincter at the bladder-urethra junction – External urethral sphincter – voluntary sphincter surrounding the urethra as it passes through the urogenital diaphragm – Levator ani muscle – voluntary urethral sphincter . Urethra The female urethra is tightly bound to the anterior vaginal wall Its external opening lies anterior to the vaginal opening and posterior to the clitoris The male urethra has three named regions – Prostatic urethra – runs within the prostate gland – Membranous urethra – runs through the urogenital diaphragm – Spongy (penile) urethra – passes through the penis and opens via the external urethral orifice Chapter 25: Urinary System 34 . 18a. b Figure .Urethra Chapter 25: Urinary System 3525. Micturition (Voiding or Urination) The act of emptying the bladder Distension of bladder walls initiates spinal reflexes that: – Stimulate contraction of the external urethral sphincter – Inhibit the detrusor muscle and internal sphincter (temporarily) Voiding reflexes: – Stimulate the detrusor muscle to contract – Inhibit the internal and external sphincters . potassium. and bicarbonate ions Abnormally high concentrations of any urinary constituents may indicate pathology . and sulfate ions – Calcium.Chemical Composition of Urine Urine is 95% water and 5% solutes Nitrogenous wastes include urea. and creatinine Other normal solutes include: – Sodium. magnesium. phosphate. uric acid. ACUTE KIDNEY INJURY WIDODO RSUP WAHIDIN sUDIROHUSODO MAKASSAR . memberi bobot yg cukup besar terhadap disfungsi ginjal .Pendahuluan Gagal ginjal akut (ARF) Salah satu kondisi yang paling sering terjadi pada kasus-kasus trauma dan penyakit kritis. Sistem scoring keparahan penyakit seperti APACHE III dan SOFA. Pendahuluan Disfungsi Ginjal ARF paling sering terjadi ICU dan sering merupakan bagian dari disfungsi organ lainnya • Berat • Memerlukan RRT • Ringan Perubahan kecil nilai kreatinin atau produksi urin Mempengaruhi morbiditas dan mortalitas pasien . Pendahuluan Jaringan Kolaborasi berbagai kelompok : ADQI= the Acute Dialysis Quality Initiative ASN = American Society of Nephrology NKF = the National Kidney Foundation dan European Society of Intensive Care Medicine AKIN the Acute Kidney Injury Network AKI . DEFINISI Acute Kidney Injury Belum ada konsensus terhadap berapa besar disfungsi ginjal yg dsb AKI. ADQI klasifikasi Risk. Failure. Loss and End Stage Kidney RIFLE . Injuri. DEFINISI mendefenisikan 3 tingkatan keparahan Risk ( kelas R ) Injuri ( Kelas I ) Failure ( Kelas F) Loss dan End Stage Kidney Disease Risiko disfungsi ginjal Sdh terjadi injuri pd ginjal Gagal ginjal kelas outcome Kelas Tingkatan . Kellum JA. Skema klasifikasi AKI berdasarkan kriteria RIFLE (dikutip : Belomo A.Gambar 1.8:R204-R212 ) .ARCritical care 2004.et al. Ronco C. 73 m2) = 186 x (Scr) .0.DEFINISI Pasien Masuk RS Tidak ada data awal fungsi ginjal Usul ADQI Asumsi GFR awal normal Gunakan Nilai Kreatinin Serum 75-100 ml/menit per 1.0203 x (0.1.742 Perempuan )x(1.210 Kulit hitam ) Rumusan MDRD ini hanya dipakai untuk memperkirakan kreatinin serum baseline .54 x (umur) .73m2 Rumus MDRD untuk perhitungan GFR Modification of Diet in Renal Disease GFR perkiraan 75(ml/min per 1. 1 (97) 0.8 (71) Tabel 1.2 (106) 1.5 (133) 1.Age (years) Black males (mg/dl [μmol/l]) Other males (mg/dl [μmol/l]) Black females (mg/dl [μmol/l]) Other females (mg/dl [μmol/l]) 20–24 1.0 (88) 0.2 (106) 1.5 (133) 1.9 (80) 40–54 1.1 (97) 1.3 (115) 1.9 (80) 55–65 1.0 (88) 30–39 1.2 (106) 1.3 (115) 1.1 (97) 1.1 (97) 1.0 (88) 25–29 1.0 (88) 0.8 (71) >65 1. Perkiraan kreatinin serum baseline .0 (88) 0.3 (115) 1.9 (80) 0.4 (124) 1.2 (106) 1. 3mg/dl (≥26.5 ml/kg per jam selama lebih dari 6 jam .5 kali base line) atau berkurangnya urin output (oligurio kurang dari 0.DEFINISI AQDI AKIN Berkurangnya fungsi ginjal secara mendadak (dlm 48 jam) yg didefenisikan sebagai peningkatan kreatinin serum lebih dari atau sama dengan 0.atau peningkatan persentase kreatinin serum lebih dari atau sama dengan 50% (1.4 umol/l). 2umol/l Memerlukan RRT Termasuk AKI Termasuk AKI Stadium I AKI Stadium III .DEFINISI AKIN Mengusulkan penyempurnaan kriteria RIFLE Penelitian Terbaru Perubahan Kecil Kreatinin Serum Berhubungan dengan ↑ mortalitas < 48 jam Kreatinin ≥ 26. Kriteria Urin Output <0.5 mL/kg/h ≥ 6 jam <0.2umol/L atau ≥150-199%(1.DEFINISI <0.9kali)baseline Stage 2 Peningkatan Cr serum 200-299%(>2-2.9 kali) baseline Stage 3 Peningkatan Cr serum ≥354umol/L dengan peningkatan sekurangnya 44umol/L atau dimulainya RRT <0.5Stage 1 1.5 mL/kg/h ≥24jam atau anuria ≥ 12 jam.5 mL/kg/h ≥12jam <0.5 mL/kg/h ≥ 6 Peningkatan Cr serum≥1.5x baseline atau penurunan GFR≥25% jam Risk Peningkatan Cr serum≥ 2 x baseline atau penurunan GFR≥50% Injury Peningkatan Cr serum≥ 3 x baseline atau penurunan GFR≥ 75% Failure atau Cr ≥ 354umol/L dengan peningkatan akut sekurangnya 44umol/L AKIN Kriteria kreatinin serum Kriteria Peningkatan Cr serum ≥ 26.5 mL/kg/h ≥12jam <0.5 mL/kg/h ≥24jam atau anuria ≥ 12 jam Tabel 2: Perbandingan Definisi dan Skema Klasifikasi AKI berdasarkan RIFLE dan AKIN . Mereka secara bermagna memerlukan dialisis dan lama perawatan lbh lama dibandingkan pasien tanpa AKI penelitian secara kohor pd 471 pasien yd dirawat di ICU selama 1 thn oleh Barrantes dkk .123 pasien sakit kritis oleh Bangshaw dkk pasien yg memenuhi defenisi AKI memiliki 3 kali kecenderungan mati selama perawatan di RS.DEFINISI Perbandingan Kriteria AKIN & RIFLE AKIN tdk lbh sensitif dari pd RIFLE dlm mendiagnosis AKI dlm 24 jam pertama di ICU penelitian multisenter terhadap 120. 7% RIFLE Injury dan 28. 26.000 populasi AKI di USA periode penelitian 15 tahun 4 kali lipat dari 610 menjadi 2880 pasien AKI di Australia 18% AKI di AS 12.000 populasi ARF yang memerlukan RRT 20 tahun terakhir 4 27 per 100.4% masuk kategori RIFLE Risk.EPIDEMIOLOGI AKI berat perlu RRT ARF 20 terakhir & tahun 5% di ICU 61 288 per 100.1% RIFLE Failure . pembuluh darah dan interstisial. . Jika sdh terjadi kerusakan pada struktur nefron sprti: glomerulus.ETIOLOGI Bersifat fungsional dan secara definisi tidak disertai perubahan histopatologi. Terjadi pd obstruksi traktus urinarius.tubulus. Nefritis intersisial Tabel 3.ETIOLOGI Pre Renal Volume responsive Intrinsik Post renal Hipovolemia Glomerular Obstruksi -Muntah dan diare -Glomerulonefritis -Batu ginjal -Perdarahan Glomerular endothelium -Fibrosis retroperitoneal Berkurangnya volume -Vaskulitis -Hypertrophy prostat sirkulasi efektif -HUS -Carcinoma -Gagal jantung -Hipertensi maligne -Striktur uretra -Septic shock Tubular -Neoplasma bladder -Sirosis -ATN -Neoplasma pelvis Obat .ACE inhibitors . Penyebab AKI .Rhabdomyolisis -Neoplasma retroperitoneal .Myeloma Intersisial . Kematian di RS dgn RIFLE •Klas R 8. •Klas I 11. .OUTCOME 19 – 83%. • Mortalitas yang lebih besar dari populasi secara umum ( 28.3% •Pasien tanpa AKI 5.4%. •Klas F 26.1%) • Pemulihan fungsi ginjal menjadi salah satu outcome Yang penting untuk dievaluasi .8%.5% Lama Perawatan ICU dan RS Pasien dengan AKI memiliki lama perawatan di ICU dan rumah sakit yang lebih lama jika dibandingkan dengan pasien tanpa AKI Morbiditas End Stage • Biaya yang mahal • Menurunnya kualitas kesehatan seseorang. . 4. 3. Tidak ada konsensus kapan dan jenis dialisis apa yang tepat untuk penderita AKI. Penyebab AKI yang multifaktorial 2. Penilaian penurunanGFR yang tergantung pada perubahan kreatinin serum.PENATALAKSANAAN Konsensus Mengenai Terapi AKI Yang Efektif Belum ada karena: 1. Bervariasinya definisi AKI. Tingginya angka mortalitas AKI 5. PENATALAKSANAAN Penelitian pd Hewan agent yg terbukti efektif utk AKI Penelitian secara Loop diuretik klinis tidak ada yg Low-dose dopamin terbukti efektif ANP Hormon tyroid IGF-1 . permeabiltas air membran. .PENATALAKSANAAN Renal Replacment Therapy (RRT) ◦ Pengganti ginjal ( Renal Replacement) ◦ Pendukung fungsi ginjal/organ lainnya (Renal/multi-organ support ◦ Berdasarkan mekanisme pengeluaran cairan/solud dan Intermitten atau Kontinyu ◦ Semua RRT kecuali PD dicapai dengan Ultrafiltrasi • Gradient tekanan akan mendorong cairan melewati membran semipermiabel. dan luas permukaan membran. • Laju UF dipegaruhi oleh: gradien tekanan trensmembran. PENATALAKSANAAN Renal Replacment Therapy (RRT) Berdaarkan mekanisme utama removal solute difusi dan konveksi Removal solute yang Predominan pada masing-masing jenis RRT 1. 3. 2. Intermittent haemodialysisi ( IHD) – difusi Continous venovenous haemofiltration (CVVH) – konveksi Continous venovenous haemodialysis ( VVHD) – difusi Continous venovenous haemodiafiltration (VVHDF) – difusi dan konveksi . 4. 5 mmol/L atau peningkatan yang cepat 6.Bellomo ) untuk memulai RRT pada AKI . Na < 110 dan > 160 mmol/l 9. Overdosis obat/ toksin yang dialyzable Jika ada satu kriteria. Creatinin > 400 umol/l 5. Jika ada dua kriteria secara bersamaan. Temperatur > 40C 10.Indikasi modern (R. Asidosis metabolik yang tak terkompensasi ( pH<7. Oliguria Anuria ( UO : 0-50 ml/12jam) 3. Komplikasi uremia : ( ensefalopati. Udem pulmo yang refrakter dengan diuretik 7. neuropati dan perikarditis) 11. RRT sangat dianjurkan Tabel 4. RRT harus dipertimbangkan.PENATALAKSANAAN Renal Replacment Therapy (RRT) (UO < 200 ml/12 jam Inisiasi:1.1) 8. K > 6.miopati.2. Urea > 35 mmol/l 4. PENATALAKSANAAN Renal Replacment Therapy (RRT) Grade D Grade E Grade C Tetapi pada kebanyakan kasus. kadar kalium ataupun derajat asidosis tergantung kondidi klinis pasien. jumlah urin. RRT dimulai sebelum urea mencapai 20-30 mmol/L). . RRT harus dimulai berdasarkan balans cairan. PENATALAKSANAAN Renal Replacment Therapy (RRT) Pilihan Metode RRT Mekanism IHD CRRT SLED Ultrafiltrasi Ultrafiltrasi Ultrafiltrasi removal cairan Mekanisme removal Difusi solute Difusi dan atau Difusi konveksi Blood Flow rate ≥ 200 ml/menit < 200 ml/menit 200 ml/menit Dialysate flow rate ≥ 500 ml/menit 17-34 ml/menit 300 ml/menit Durasi 3-4 jam 24 jam/ hari 6-12 jam/hari . PENATALAKSANAAN Renal Replacment Therapy (RRT) Keuntungan dan pertimbangan khusus IHD Removal cairan yang cepat √ Bersihan solute cepat √ Hiperkalemia berat CRRT SLED √ Hempdinamik tak stabil √ √ Kontrol cairan lebih baik √ √ -High nutritional Support √ -Removal solute MMW √ ? . Chronic Kidney Disease . Also. the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) Advisory Board approved development of clinical practice guidelines to define chronic kidney disease and to classify stages in the progression of chronic kidney disease. there is an increasing prevalence of earlier stages of chronic kidney disease which unfortunately is “underdiagnosed” and “under-treated” in the United States. .000 of these are on dialysis. there is a rising incidence and prevalence of Kidney Disease.Chronic Kidney Disease In the United States. In 2000. Nearly 350. Stages of Chronic Kidney Disease Stage 1 Kidney damage with normal or ↑ GFR GFR ≥ 90 ml/min/1.73 m2 Stage 2 Kidney damage with mild ↓ GFR GFR 60-89 Stage 3 Moderate ↓ GFR GFR 30-59 Stage 4 Severe ↓ GFR GFR 15-29 Stage 5 Kidney failure GFR <15 (or dialysis) . Causes of End Stage Renal Disease USRDS Annual Data Report . . – – – – – – Chronic Renal Insufficiency Chronic Renal Failure Renal Insufficiency Pre dialysis renal disease Pre uremia Renal dysfunction They are imprecise & poorly defined.Chronic Kidney Disease Many terms are used to describe states of reduced glomerular filtration (GFR) not requiring renal replacement therapy. – Creatinine Clearance calculated by timed (24h) urine collection along with serum collection for Creatinine. . Estimation of GFR – More than 10 formulae for estimation of GFR. – This factor can be corrected by cimetidine. – Overestimate GFR when CKD is severe due to an increase in tubular secretion of creatinine.Chronic Kidney Disease Measurement of GFR – Gold standard is Inulin Iothalamate. – MDRD most widely accepted now. CKD – Risk Factors Diabetes Mellitus Hypertension Cardiovascular Disease Obesity Metabolic Syndrome Age and Race Acute Kidney Injury Malignancy Family history of CKD Kidney Stones Infections like Hep C and HIV Autoimmune diseases Nephrotoxics like NSAIDS . Causes Diabetic Non Diabetic – Glomerular Nephritic: PIGN. Ch. Obs Vascular: Vasculitis. RAS Cystic: ADPKD CKD in transplantation . Membranous.CKD . HTN. Reflux. IgA. MPGN Nephrotic: FSGS. Amyloidosis – – – – Tubulointerstitial: Analgesic. Causes .CKD . CAUSES OF DEATH IN ESRD U. Renal Data System: USRDS 2002 .S. CKD . Hypertension Abnormal Acid-base abnormalities – Metabolic Acidosis due to uremia or RTA Abnormal hematopoesis – Anemia of CKD Cardiovascular Abnormalities – LVH. pruritus.Manifestations Abnormal Sodium-Water metabolism – Edema. CAD. arthralgia – Hyperparathyroidism – Renal Osteodystrophy . Diastolic Dysfunction Abnormal Calcium-Phosphorus metabolism – Hyperphosphatemia. CKD .Management Diagnostic work up to decide underlying etiology Treatment of Hypertension and Dyslipidemia Treatment of Anemia Treatment of Hyperphosphatemia Avoidance of Dehydration & Nephrotoxic agents Proper Dosing of Drugs Preparation for Renal Replacement Therapy . Evaluation .CKD . UPEP Kidney Ultrasound Urine sediment analysis Biopsy – Evidence of glomerular disease without diabetes – Sudden onset of nephrotic syndrome or glomerular hematuria . C4 SPEP.Evaluation Serum electrolytes Urine spot protein analysis (24 hour no longer recommended).CKD . C3. ANA. – Decrease the sodium intake to 2. – ACEIs and ARBs have been demonstrated to slow both diabetic and non-diabetic renal disease in both experimental and human studies.CKD . .5 g /day – Usually requires more than 2 medications. – Diuretics enhance the antihypertensive and antiproteinuric effects of other agents.Hypertension Anti-Hypertensive Agents – Single most important measure could be adequate BP control – Target BP <130/80 with minimal proteinuria and BP<125/75 with significant proteinuria (>1g).. CKD .Dyslipidemia Dyslipidemia and Cardiovascular morbidity – Several studies like the 4D study showed no benefit of statins in dialysis patients. – However. – Dyslipidemia is frequently seen in glomerular disease with proteinuria (nephrotic syndrome) and its control reduces atherosclerosis related morbidity and mortality. post hoc analysis of this data does suggest that the management of dyslipidemia in CKD 2 – 4 improves cardiac mortality and morbidity. . Due to decrease in EPO production in the kidney. Mostly apparent in the stage 4 and 5 of CKD. . Diagnosis of exclusion.CKD .Anemia Decreased quality of life with anemia. CKD . Sufficient Iron should be administered to correct iron stores. Epogen® – Darbepoietin Alpha: ARANESP ® Target Hg levels between 11g and 12g but not exceeding 13g.Anemia Erythropoietin – Epoetin alfa :Procrit ® . Greater than 13g showed increased mortality as per the CHOIR study. . Ca-acetate (PHOSLO) Lanthanum Renagel .CKD . calcification in synovial membranes.Hyperphosphatemia Control of Hyperphosphatemia – Due to decreased excretion in urine. Calcium Carbonate (TUMS). – Therapy includes Phosphorus restriction to 800mg/day and use of phosphrous binders with food. – Hyperphosphatemia leads to pruritus. blood vessels and even cardiac valves. – Control of hyperphosphatemia by dietary measures slow progression in experimental models of CKD. – Calcimimetic agents like cinacalcet.CKD – Bone and Mineral disease Hyperparathyroidism: – High phosphorus and low Vitamin D causing low calcium. – Vitamin D analog paricalcitol. – Maintain Phosphorus and Calcium within normal ranges. . – Monitor Intact PTH levels and keep between 100 and 500. even in absence of renovascular disease. ACEIs or ARBs can aggravate renal dysfunction – Dehydration is frequent in tubulo-interstitial disorders where urinary concentration is impaired. Allopurinol . – Proper Dosing of Drugs eg. In presence of dehydration.Nephrotoxics Avoidance of Dehydration/Nephrotoxic Agents – – – Drugs such as Aminoglycosides. NSAIDs Avoiding exposure to Radio contrast agents.CKD . CKD – Medication Dosing Proper Dosing of Drugs – – – – Uremia affects GI absorption. eg Iron. Impaired plasma protein binding of drugs. Some drugs used in normal dose will lead to nephrotoxic effects eg. Increased volume of distribution. Vancomycin. Allopurinol Other drugs when used in normal dose will lead to other toxic effects eg. Dose Reduction or Interval Extension . eg Dilantin. Excretion of many drugs depends upon the kidney. – Timely placement of vascular access or PD catheter.RRT Preparation for Renal Replacement Therapy – Education for Options of Dialysis & Renal Transplantation for Renal Replacement – Hemodialysis Vs Peritoneal Dialysis – Avoidance of Veni-puncture & insertion of catheters in peripheral veins once GFR < 60mls.CKD . . vomiting and poor nutrition Metabolic acidosis Lethargy and Malaise Worsening kidney function <10 ml or <15 ml in diabetics .RRT Indications (Absolute): – – – – – Uncontrolled hyperkalemia and acidosis Uncontrollable hypervolemia (pulmonary edema) Pericarditis AMS and somnolence (advanced encephalopathy) Bleeding diathesis Indications (Relative): – – – – Nausea.CKD . CKD .RRT Transplantation: – Preemptive transplant carries both patient and graft survival advantage. – Graft survival better with living donor kidneys. . – Immunosuppresion is almost always a must. RRT Transplantation: – Diseases like FSGS may reccur early in the transplanted kidney. bone loss. cardiovascular disease. – Increased risk for infection.CKD . – Contraindications: Malignancy (recent or metastatic) Current infection Severe extra renal disease Active use of illicit drugs .