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The lines of defense for maintenance of blood pH after ingesting an acid load are four-fold, taking effect over different time scales. What are they, and what are the time scales?

1. Plasma bicarbonate neutralizes protons, producing CO2 via carbonic anhydrase (immediate). 2. Increased respiratory drive results in expulsion of excess CO2 (within minutes). 3. Intracellular ion exchange (H+ exchange for Na+ or K+) and bone-derived phosphate further buffer excess protons (within hours). 4. Kidney retention of bicarbonate and excretion of organic acids completes the response (within days).


What is the definition of metabolic alkalosis? What are three causes of metabolic alkalosis?

Metabolic alkalosis increase in serum bicarbonate levels resulting in elevated pH. Causes can be broken into three groups: i) bicarbonate ingestion, e.g. lots of exogenous supplemented NaHCO3, ii) gastric acid loss resulting in less H+ to be buffered by plasma HCO3-, e.g. vomiting, iii) renal loss of HCO3-, e.g. loop/thiazide diuretics or genetic tubular defects


What is the typical approach to manage a patient with hypotonic hyponatremia? What role does the patient's volume status play?

If a patient is hypovolemic, normal saline is given; if a patient is hypervolemic, treating the primary disease is the priority. In general, water is restricted to allow pure water evaporation, plasma sodium correction occurs at no more than 8 mEq/d, and more aggressive options (e.g. hypertonic saline or V2R antagonists) are reserved for patients who are symptomatic or severely hyponatremic.


Should patients with CKD on dialysis strive for over-consumption or restriction of sodium, potassium, and phosphorus? How common are vitamin deficiencies in patients on dialysis?

Sodium, potassium, and phosphorus restriction are recommended for patients with CKD. Dialysis is a protein and vitamin-losing state -- deficiencies are very common! High protein diets are often recommended for dialysis patients as well as "renal vitamin" supplementation. Note that highly restrictive diet options are often weighed vs. patient preferences and comorbidities (e.g. lean body mass loss) in patients with severe kidney disease.


What differentiates normal saline from lactated ringers? What is the critical thing that distinguishes both of these from D5W, and when would you use D5W vs. either isotonic saline or lactated ringers?

Lactated ringers is more precisely isotonic (normal saline slightly hypertonic) – but the main difference from normal saline is that lactated ringers also contains lactate, potassium, and calcium. The lactate can thus be good for preventing a metabolic alkalosis if that is a concern. However, isotonic and ringers can both be used for volume expansion because they have similar Na concentrations to plasma and thus the fluid will remain in the extracellular space. D5W, on the other hand, has no sodium and is thus a good option for addressing a pure water deficit in a patient who has plenty of sodium.


Chronic injury to the kidney results in the death of nephrons. However, until CKD is severe, GFR is largely maintained. What changes occur which attempt to repair the kidney and restore GFR?

Physical factors related to blood flow and activation of the renin angiotensin system increase the workload of individual surviving nephrons, and these nephrons will undergo work-related hypertrophy. This increases metabolic requirement of individual nephrons, however, which can be maladaptive.


Which renal syndrome is associated with massive protein loss in the urine? How might this cause some clinical findings of this syndrome, such as edema?

Nephrotic syndrome (proteinuria >3g/d). Hypoalbuminemia and low protein content in the plasma reduces plasma oncotic pressure, favoring fluid movement into the interstitial space (EDEMA). Protein loss can also cause hypocoagulability (loss of coagulation factors) or predispose to infection (loss of antibodies). Hyperlipidemia is also a defining factor of nephrotic syndrome and relates to the liver's adaptive response (biosynthesis) to protein and lipid loss in the urine.


How does your management of a chronic kidney disease patient differ by CKD stage?

Stage 1,2: diagnose, delay progression, reduce CV risk, reduce proteinuria. This includes blood pressure management and RAAS inhibition, glycemic control, dietary changes. Stage 3: same as before, but begin to assess for complications. Stage 4: same, but more frequent assessment for complications. Discuss renal transplant or dialysis. Stage 5: prepare for transplant and/or initiate dialysis.


How does the GFR change during the natural history of diabetic nephropathy? What about the kidney biopsy? Hint: consider an early, middle, and late phase of diabetic nephropathy.

During the hyperfiltration/silent phase, GFR increases and the basement membrane thickens. During the microalbuminuria/incipient nephropathy phase, GFR drops back down to "normal" and the biopsy shows mesangial matrix expansion (a hallmark of diabetic nephropathy) in addition to glomerulosclerosis. During the macroalbuminuria phase, GFR drops rapidly and ESRD will often occur within 10 years. The biopsy may worsen but will retain the characteristics seen in the incipient nephropathy phase.