#64 – KDIGO Guidelines



***LISTEN TO THE PODCAST HERE***



What are KDIGO and KDOQI???

  • The 2 Organizations
    • Kidney Disease Outcomes Quality Initiative (KDOQI)
      • US Based
      • Developed in 1997 by National Kidney Foundation
    • Kidney Disease: Improving Global Outcomes (KDIGO)
      • Global organization developing and implementing evidence based clinical practice guidelines in kidney diseases
      • Developed in 2003 by NKF
    • Essentially individual entities, but both comment various aspects of kidney diseases
  • 2012 Guidelines
    • Published by KDIGO and commented by KDOQI
    • 5 chapters


Chapter 1: Definition and Classification of CKD

  • Definition
    • Abnormalities in kidney structure or function, present for > 3 months, with implications on health
  • Staging
    • Based on causes, GFR category, and albuminuria category
  • Predicting Prognosis of CKD
  • Evaluation of GFR
    • Recommend using serum creatinine and GFR estimating equation for initial assessment
    • Recommend only using cystatin C in adult patients with decreased GFR but without markers of kidney damage if diagnosis of CKD is required
  • Evaluation of Albuminuria
    • Initial testing for proteinuria should be an early morning urine sample(in descending order of preference):
      • Urine albumin-to-creatinine ratio (ACR)
      • Urine protein-to-creatinine ratio (PCR)
      • Reagent strip urinalysis for total protein with automated reading
      • Reagent strip urinalysis for total protein with manual reading
    • Microalbuminuria should no longer be used by laboratories
    • If ACR > 30mg/g, then proceed to confirm with a random untimed urine sample

Chapter 2: Definition, Identification, and Predication of CKD Progression

  • Assess albuminuria at least annually
  • CKD progression is based on the one of the following:
    • Decline in GFR category
    • Drop in eGFR by ≥ 25% of baseline
    • Sustained decline in eGFR by > 5mL/min/year
  • Identify known risk factors associated with CKD progression
    • Cause of CKD
    • Age
    • Gender
    • Hypertension
    • Hyperglycemia
    • Dyslipidemia
    • Smoking
    • Obesity
    • History of CVD
    • Ongoing exposure to nephrotoxic agents

Chapter 3: Management of Progression and Complication of CKD

  • Hypertension
    • BP ≤ 140/90 if urine albumin excretion < 30mg/d
    • BP ≤ 130/80 if urine albumin excretion > 30mg/d
    • Recommend ACEI or ARB
  • Protein Intake
    • Recommend protein intake 0.8g/kg/d
  • Glycemic Control
    • Recommend HbA1C AROUND 7.0%
    • ***newer ACE guidelines recommend < 6.5% with SGLT2i**
  • Recommend < 2g/day
    • Lifestyle
      • Recommend 30 min/day five times per week, smoking cessation, and healthy weight (BMI 20-25)
  • Complications Associated with CKD
    • Anemia
      • Diagnosed at < 13g/dL in men and < 12 g/dL in women
      • Screening in patients with CKD:
        • Stage G1-2 – when clinically indicated
        • Stage 3a-3b – at least annually
        • Stage 4-5 – at least twice per year
    • Metabolic Bone Disease
      • Obtained baseline calcium, phosphate, PTH, and ALP at least once in patients with GFR < 45 mL/min
      • Not recommended to screen with bone mineral density testing
      • Not recommended to supplement vitamin D of bisphophonates with deficiency or strong clinical rationale
    • Acidosis
      • Supplement oral bicarbonate in patients with serum bicarbonate < 22 mmol/L

Chapter 4: Other Complications of CKD

  • CVD
    • All CKD patients are at increased risk for CVD
    • Recommend same testing and treating as non-CKD patients
    • Use caution when interpreting NT-proBNP and troponins
  • PVD
    • Recommend regular podiatric assessment
  • Medication Management
    • Recommend using GFR for dosing adjustments
      • Example – Metformin
        • Stage G1-3a – continue
        • Stage G3b – monitored
        • Stage G4-5 – discontinued
  • Imaging studies and radiocontrast
    • Avoid if possible, but do not hold if needed
    • Following KDIGO Clinical Practice Guidelines for AKI
      • Avoid high osmolar agents
      • Use lowest contrast dose possible
      • Stop nephrotoxic agents before and after
      • Maintain adequate hydration
      • Measure GFR 48-96 hours after

Chapter 5: Referral to Specialist and Models of Care



Cottage Physician (1893)



References

  1. KDIGO. Clinical Practice Guideline for the Evaluation and Management of CKD. 2012.
  2. Inker LA, Astor BC, Fox CH, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD. Am J Kidney Dis. 2014; 63(5):713-35. [pubmed]
  3. Stevens PE, Levin A. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013; 158(11):825-30. [pubmed]
  4. Andrassy KM. Comments on ‘KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease’. Kidney Int. 2013; 84(3):622-3. [pubmed]

PAINE #PANCE Pearl – Surgery



Question

Surgery is a major physiologic stress and often is accompanied by biochemical derangements that effect homeostasis in the post-operative period. Describe the most common clinical scenarios that can cause each of the four main acid-base imbalances in a post-surgical patient.



Answer

  • Metabolic Acidosis
    • Lactic acidosis (HAGMA)
      • Under-resuscitation
      • Blood loss
    • Hyperchloremia (NAGMA)
      • High chloride load from NaCl
  • Metabolic Alkalosis
    • Volume contraction and bicarbonate reabsorption
    • GI loss from NG tube suction or emesis
  • Respiratory Acidosis
    • Opioid medications causing depressed respiratory drive
  • Respiratory Alkalosis
    • Splinting from pain

PAINE #PANCE Pearl – Renal



Question

42yo woman, with a history systemic lupus erythematosus, presents to your clinic with a 1-month history of progressive leg swelling and polyuria. She is complaint with her medications and states that she hasn’t changed anything in her medical care. Physical examination reveals 2+ pitting edema to the knees in the lower extremities. BMP, UA, and urine microscopy are below.

  1. What is the next step in diagnosing this patient and what would you expect to find?


Answer

This patient found to heavy proteinuria on a urinalysis and oval fat bodies on urine microscopy, which would point to nephrotic syndrome as a diagnosis.

The next step in the diagnostic management of this patient would be to perform a 24-hour urine collection for urine protein. Normal urine protein excretion is < 150mg/day, but nephrotic range proteinuria is diagnostic at > 3.5g/day. Alternatively, a random urine protein-to-creatinine ratio of > 3.5 can be used, but is less reliable than a 24-hour collection.

Once a nephrotic syndrome diagnosis is made by urine studies, it should be followed up with a renal biopsy to determine the cause.

#51 – Renal Tubular Acidosis



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Definition

  • Group of disorders that cause a metabolic acidosis due to defects in the renal tubules
    • Net retention of HCl
    • Net loss of NaHCO3

Pathophysiology

The kidney regulates acid-base balance two main ways:

  • Reabsorption of filtered HCO3
    • >80% of the bicarbonate filtered by the glomerulus is reabsorbed in the proximal renal tubules via Na-H exchange
  • Acid excretion
    • Collecting ducts of the nephron excrete hydrogen ions buffered by NH3 and PO3 (so the pH of the urine doesn’t destroy the nephron)
      • Extra production of NH3 is stimulated by intracellular acidosis.
  • 3 step process
    • Reabsorption of sodium to create a negative gradient in the tubular lumen
    • Excretion of hydrogen by H-K-ATPase and reabsorption of potassium
    • Prevention of hydrogen ions from diffusing back out of the tubular lumen

Initial Presentation

  • Patients diagnosed with an RTA must first be diagnosed with a metabolic acidosis
    • Decreased pH with decreased HCO3
  • After this is determined, the anion gap must be calculated and found to be normal
    • AG = Na – (Cl + HCO3) = 8-12

Differential for NAGMA

  • Ureteric diversion
  • Small bowel fistulae
  • Excessive saline
  • Diarrhea
  • Carbonic anhydrase inhibitors
  • Renal tubular acidosis
  • Adrenal insufficiency
  • Pancreatic fistulae

Type I (distal) RTA

  • Cause
    • Defect in the distal hydrogen ion excretion
  • Pathophysiology
    • Failure of the H-ATPase proton pump (most common cause)
      • Inability to acidify urine < 5.5
      • Hypokalemia
    • Increased hydrogen ion permeability of the luminal membrane

Type II (proximal) RTA

  • Cause
    • Defect in proximal bicarbonate reabsorption
  • Pathophysiology
    • Damage to the proximal tubule that leads to progressive bicarbonate wasting in the urine

Type IV (hypoaldosteronism)

  • Cause
    • Reductions in aldosterone secretion and responsiveness
  • Pathophysiology
    • Decreased rate of proton secretion rather than an intrinsic defect in the tubule’s capacity to generate normal pH gradient
    • Hyperkalemia causes reduced urine NH4, which in turns leads to more acidic urine
      • Hydrogen ions have nothing to bind to

Diagnostic Work-Up

  • RTAs should be considered in any patient with a normal anion gap metabolic acidosis
    • Need ABG and BMP
  • Once this determination is made:
    • Urine pH
      • > 5.5 in type I (distal)
      • < 5.5 in type II (proximal) and type IV
    • Urine ammonium
      • Elevated in type II (proximal)
      • Decreased in type I (distal) and type IV
      • Most labs can’t measure urine ammonium directly:
        • Urine Anion Gap (urine Na+K+Cl)
          • (+) UAG = > 20
            • Type I (distal) and type IV
          • (-) UAG = < – 20
            • Type II (proximal)
    • Serum potassium
      • Elevated in type IV
      • Decreased in type I and II

Treatment

  • Type I (distal)
    • Urinarary Alkali Therapy
      • Sodium bicarbonate
        • Increased risk of nephrolithiasis due to bicarbonaturia
          • Use potassium citrate instead
  • Type II (proximal)
    • Much more difficult to treat due to the INCREASED bicarbonate diuresis during bicarbonate therapy
    • Alkali therapy (10x the dose for type I) AND potassium salt repletion as bicarbonaturia INCREASES urinary potassium losses
    • Thiazide diuretics if large alkali doses ineffective or not tolerated
      • Diuresis reduces urinary bicarbonate loss by increasing proximal sodium reabsorption
        • Which secondarily increased bicarbonate reabsorption
  • Type IV
    • Stop any medication causes or treat underlying condition (hypoaldosteronism)
      • Mineralcorticoid (fludrocortisone) and glucocorticoid (hydrocortisone)
    • Potassium repletion
Up-To-Date. 2019



References

  1. Rodríguez Soriano J. Renal tubular acidosis: the clinical entity. Journal of the American Society of Nephrology : JASN. 2002; 13(8):2160-70. [pubmed]
  2. Skelton LA, Boron WF, Zhou Y. Acid-base transport by the renal proximal tubule. Journal of nephrology. ; 23 Suppl 16:S4-18. [pubmed]
  3. Hamm LL, Nakhoul N, Hering-Smith KS. Acid-Base Homeostasis. Clinical journal of the American Society of Nephrology : CJASN. 2015; 10(12):2232-42. [pubmed]
  4. The Curbsiders.  Episode 104. https://thecurbsiders.com/internal-medicine-podcast/104-renal-tubular-acidosis-kidney-boy-joel-topf-md
  5. DB’s Medical Rants.  http://www.medrants.com/archives/8897
  6. Oh M, Carroll HJ. Value and determinants of urine anion gap. Nephron. 2002; 90(3):252-5. [pubmed]
  7. Rodríguez Soriano J. Renal tubular acidosis: the clinical entity. Journal of the American Society of Nephrology : JASN. 2002; 13(8):2160-70. [pubmed]
  8. Karet FE. Mechanisms in hyperkalemic renal tubular acidosis. Journal of the American Society of Nephrology : JASN. 2009; 20(2):251-4. [pubmed]

PAINE #PANCE Pearl – Renal



Question

42yo woman, with a history systemic lupus erythematosus, presents to your clinic with a 1-month history of progressive leg swelling and polyuria. She is complaint with her medications and states that she hasn’t changed anything in her medical care. Physical examination reveals 2+ pitting edema to the knees in the lower extremities. BMP, UA, and urine microscopy are below.

  1. What is the next step in diagnosing this patient and what would you expect to find?

Ep-PAINE-nym



Loop of Henle

Other Known Aliasesansa nephroni

Definitionportion of the nephron that goes from the proximal convoluted tubule to the distal convoluted tubule. There are four portions of this structure:

  • Thin descending segment
  • Thin ascending segment
  • Ascending limb
  • Cortical thick ascending limp

Clinical Significance the loop of Henle creates an area of high urea concentration with secretion and reabsorption of water and electrolytes. This is also the portion of the nephron where the aptly named “loop diuretics” to manage blood pressure by means of excess fluid excretion.

HistoryNamed after Friedrich Gustav Jakob Henle (1809-1885), who was a German physician, pathologist, and anatomist and received his medical doctorate from the University of Bonn in 1832. He spent his early career as a prosector for Johannes Müller in Berlin where he published furiously on numerous facets of human and animal anatomy and physiology. He then went on to become the chair of anatomy at the University of Zurich, where he became one of the early adopters and advocates for the study of pathophysiology as a single distinct discipline. He also set the early argument for the germ theory in an essay entitled “On Miasma and Contagia”. His life’s work culminated in the publishing of the Handbook of Systematic Human Anatomy in 1855, which was the most complete and comprehensive work at that time.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com

#43 – ABG Interpretation



Ground Rules

  1. Accurate assessment of a patient’s acid/base status requires a measurement of arterial pH and PCO2
    1. bedside analyzers directly measure these and then use the Henderson-Hasselbach equation to calculate the HCO3-
    2. You can use venous blood, but must make adjustments:
      1. pH is 0.03-0.04 lower than arterial
      2. PCO2 is 7-8 mmHg higher than arterial
      3. HCO3- is 2 mEq/L higher than arterial
    3. A primary disturbance is usually accompanied by a compensatory response, but does not fully correct the pH


There are four main ways pH can change:

  • Metabolic Alkalosis
    • increase in HCO3- and increase in pH
  • Metabolic Acidosis
    • Decrease in HCO3- and decrease in pH
  • Respiratory Alkalosis
    • Decrease in PCO2 and increase in pH
  • Respiratory Acidosis
    • Increase in PCO2 and decrease in pH

 

 

Remember, that the lungs can compensate considerable FASTER than the kidneys.

  • Lungs can excrete 12 moles of acid per day as CO2
  • Kidneys can excrete 0.1 moles of acid per day as ammonia, but can secrete HCO3- to buffer

 


Respiratory Acidosis

  • Decrease in minute ventilation (TV x RR)
  • Causes
    • Normal Lungs
      • CNS depression (drugs, head trauma)
      • Neuromuscular impairment (GBS, MG)
      • Thoracic restriction
    • Abnormal Lungs
      • Obstruction
      • Alveoli dysfunction (ARDS)
      • Perfusion defect (cardiac arrest, PTE)
  • Compensation
    • Acute
      • Increase of 10 mmHg of PaCO2 will increase serum HCO3- by 1 mEq/L
    • Chronic
      • Increase of 10 mmHg of PaCO2 will increase serum HCO3- by 3 mE1/L

Respiratory Alkalosis

  • Increase in minute ventilation (TV x RR)
  • Causes
    • Cardiac
    • Hypoxemia
    • Anemia
    • Medications
    • Pregnancy
    • Iatrogenic
    • Obstruction
    • Neurologic
    • Stress
  • Compensation
    • Acute
      • Decrease of 10 mmHg of PaCO2 will decrease serum HCO3- by 2 mEq/L
    • Chronic
      • Decrease of 10 mmHg of PaCO2 will decrease serum HCO3- by 4 mEq/L

If the condition is 100% acute respiratory, then the pH will change 0.08 for every 10 mmHg change in PaCO2



Metabolic Acidosis

  • Decreased pH due to decreased HCO3-
  • First step after determining that a patient has a metabolic acidosis is to calculate the anion gap
  • High Anion Gap Metabolic Acidosis (HAGMA)
    •  Causes
      • Carbon monoxide, cyanide
      • Aminoglycosides
      • Theophyline, toluene
      • Methanol
      • Uremia
      • Diabetic ketoacidosis
      • Propylene glycol
      • Inborn errors of metabolism
      • Lactic acidosis
      • Ethylene glycol, ethanol
      • Salicylates

  • Calculating a Delta Gap

  • Normal Anion Gap Metabolic Acidosis (NAGMA)
    • Causes
      • Ureteric diversion
      • Small bowel fistulae
      • Excessive saline
      • Diarrhea
      • Carbonic anhydrase inhibitors
      • Renal tubular acidosis
      • Adrenal insufficiency
      • Pancreatic fistulae

  • Respiratory Compensation
    • Expected PaCO2 = 8 + (1.5 x HCO3-) ± 2

Metabolic Alkalosis

  • Increased pH due to increased HCO3-
  • Causes
    • Contraction
    • Licorice
    • Endocrine
    • Vomiting
    • Excessive NG suction
    • Ringer’s solution
    • Post-hypercapnia
    • Diuretics
  • Respiratory Compensation
    • Expected PaCO2 = 20 + (0.7 x HCO3-) ± 5 

PAINE #PANCE Pearl – Renal



Question

 

In an oliguric patient, what is the first step in differentiating between prerenal and intrinsic renal causes?

 



Answer

 

The fractional excretion of sodium (FENa) can help differentiate prerenal from intrinsic renal causes in patient with oliguria.  If the FENa is < 1%, it suggests prerenal and if it is > 2%, it suggests intrinsic renal causes.  There are many limitations to using this calculation, but it is a good first step in determining the cause of a patient’s oliguria.  Other laboratory studies, such as BUN/Cr, can be useful as well.

 

Image result for fractional excretion of sodium

Ep-PAINE-nym



Bowman’s Capsule

 

Other Known AliasesCapsula glomeruli, glomerular capsule

DefinitionDouble walled, cup-like capsule surrounding the glomerulus

Image result for bowman's capsule

Clinical SignificanceIt is made up of two poles: a vascular pole (afferent and efferent arterioles) and a urinary pole (proximal convoluted tubule). Within the capsule, there is a parietal layer and visceral layer with a space in between.  This is where ultrafiltration takes place and urine is filtered from the blood.

History – Named after Sir William Bowman (1816-1892), who was an English ophthalmologist, histologist, and anatomist, and first identified this structure in 1841.  He published his findings at the age of 25 and was awarded The Royal Medal by the Royal Society of  London.

He was well known for his extensive use microscopes in visualizing structures of the human body and publishing two works with his mentor, Robert Bentley Todd, entitled “Physiological Anatomy and Physiology of Man” and “Cyclopaedia of Anatomy and Physiology”.

William Bowman.jpg

The Cyclopaedia Of Anatomy And Physiology


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Bowman W.  On the Structure and Use of the Malpighian Bodies of the Kidney.  Phil Trans R Soc Lond.  1842;132:57-80
  6. Eknoyan G. Sir William Bowman: his contributions to physiology and nephrology. Kidney international. 1996; 50(6):2120-8. [pubmed]
  7. Galst JM. Sir William Bowman (1816-1892). Archives of ophthalmology (Chicago, Ill. : 1960). 2007; 125(4):459. [pubmed]