Minimize Oxalate intake (for patients with calcium Oxalate stones)
Minimize animal protein intake (reducing animal protein intake has shown to reduce kidney stone risk in only men)
Increase fruit and vegetable consumption (increase in potassium has been shown to reduce stone formation especially in older men and women)
Why not reduce calcium intake? It can adversely affect bone density, especially in patients at risk of osteoporosis including women and the elderly. Reducing calcium intake can also increase the stone risk by increasing the calcium Oxalate content.
Taylor EN, Curhan GC. Diet and fluid prescription in stone disease. Kidney Int 2006; 70:835.
Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993; 328:833.
Meschi T, Maggiore U, Fiaccadori E, et al. The effect of fruits and vegetables on urinary stone risk factors. Kidney Int 2004; 66:2402.
1. Refractory Fluid Overload
2. Severe hyperkalemia (>6.5 mEq/L) or rapidly rising potassium levels
3. Signs of uremia including pericarditis, encephalopathy, or decline in mental status not explained by other abnormality/condition
4. Severe metabolic acidosis (pH<7.1)
5. Certain alcohol and drug intoxications
In patients with underlying chronic kidney disease (CKD), the likelihood of receiving dialysis increases in proportion to the decline in glomerular filtration rate (GFR) at baseline.
Pannu N, Klarenbach S, Wiebe N, et al. Renal replacement therapy in patients with acute renal failure: a systematic review. JAMA 2008; 299:793.
Gaudry S, Hajage D, Schortgen F, et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. N Engl J Med 2016; 375:122.
Calcium homeostasis is normally under very tight control! There are 3 main sites of control: the gastrointestinal tract, bone, and kidney.
Hypercalcemia can happen for a variety of reasons (Multiple myeloma, cancer, Sarcoidosis, hyperparathyroidism, Milk-alkali syndrome, vitamin D intoxication etc.)
Subsequently acute renal failure may develop in the context of this pathology for several reasons.
Polyuria during the hypercalcemia may cause hypovolemia and pre-renal AKI.
Vaso-constrictive effects of calcium. An increased influx of calcium into the vascular smooth muscle cells leads to an augmented muscular tone. Therefore increased vascular resistance and reduced renal perfusion.
Hypercalcemic nephrolithiasis. Formation of Ca2+-Oxalate stones, potentially causing obstruction and renal insufficiency.
Moysés-Neto M et al. Acute renal failure and hypercalcemia. Ren Fail. 2006;28(2):153-9.
Simonetti G. Calcium and blood pressure. Ther Umsch. 2007 May;64(5):249-52.
Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1;67(9):1959-66.
Parks J, Coe F, Favus M. Hyperparathyroidism in Nephrolithiasis. Arch Intern Med. 1980;140(11):1479-1481.
Magnesium deficiency is often associated with refractory hypokalemia (In up to 50% of cases there is concomitant hypomagnesemia).
WHY? Exact mechanism isn’t known for certain.
PROPOSED MECHANISM: Low intracellular magnesium causes renal wasting of potassium. Normally magnesium will inhibit Renal Outer Medullary Potassium (ROMK) channels in the kidneys; however, hypomagnesemia allows the ROMK channel to efflux K+ into the urine.
NOTE: High Na+ uptake/ aldosterone states may also cause K+ loss (see image).
Chou-Long Huang and Elizabeth Kuo. Mechanism of Hypokalemia in Magnesium Deficiency. JASN October 2007 vol. 18 no. 10 2649-2652
WHAT IS IT? Hyponatraemia (dilutional) secondary to excessive alcohol consumption and undernourishment (i.e low protein/salt)
HOW? Malnourished chronic alcoholics with minimal solute/ protein intake are susceptible to water toxicity at small volumes (due to loss of urea concentrating gradient) compared to healthy individuals with normal renal function (normal adults can drink up to 20L a day without subsequent hyponatremia).
*Fluid intake over 4-5 L can push them into hyponatremia [Obligatory solute loss is ~250mOsm/day]
Free water excretion from the kidney depends on both urinary dilution capacity AND solute excretion
MAX urine diluting capacity= 50 mOsm/L
Beer potomania= LOW osmoles due to poor diet
Hence the low solutes makes the kidneys HOLD onto the fluid because there are insufficient osmoles to allow for excretion of the water
So when you give solute, they undergo diuresis rapidly and are at risk of over correcting! ADH is SUPPRESSED due to all the volume retention!
Bhattarai N, Kafle P, Panda M. Beer potomania: a case report. BMJ Case Reports. 2010;2010:bcr10.2009.2414. doi:10.1136/bcr.10.2009.2414.
Sanghvi, S. R.,Kellerman, P. S. & Nanovic, L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am. J. Kidney Dis. Off. J. Natl. Kidney Found. 50,673–680 (2007).
Shalin R. Sanghvi, Paul S. Kellerman, Lisa Nanovic. Beer Potomania: An Unusual Cause of Hyponatremia at High Risk of Complications From Rapid Correction. AJKD. October 2007 Volume 50, Issue 4, Pages 673–68
Azotemia => Characterized by increased levels of nitrogen-containing compounds (i.e urea, BUN) NOT severe enough to cause symptoms.
Uremia => (“urine in the blood”) Characterized by increased levels of nitrogen-containing compounds (i.e urea, BUN) severe enough to cause symptoms. Symptoms are non-specific: fatigue, weakness, nausea, vomiting, itchiness, confusion, pericarditis, coma, etc.
Bishop, M.L.; Fody, E.P. and Schoeff, L.E. Clinical Chemistry: Techniques, Principles, Correlations. 6th Edition. Lippincott Williams and Wilkins. p. 268.
Rose BD, Post TW. Hyperkalemia. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed. New York, NY: McGraw-Hill; 2001:913-919.
Rarely, there can be purple discoloration of the urine, collecting bag, and tubing (the purple urine bag syndrome). The purple color of the urine is due to metabolic products of biochemical reactions formed by bacterial enzymes in the urine. Gastrointestinal tract flora break down the amino acid tryptophan into indole, which is subsequently absorbed into the portal circulation and converted into indoxyl sulfate. Indoxyl sulfate is then excreted into the urine, where it can be broken down into indoxyl if the appropriate alkaline environment and bacterial enzymes (indoxyl sulfatase and indoxyl phosphatase) are present. The breakdown products, indigo and indirubin, appear blue and red, respectively. Bacteria capable of producing these enzymes include Providencia spp, Klebsiella, and Proteus.
Peters P, Merlo J, Beech N, et al. The purple urine bag syndrome: a visually striking side effect of a highly alkaline urinary tract infection. Canadian Urological Association Journal. 2011;5(4):233-234. doi:10.5489/cuaj.10177.
Lin C-H, Huang H-T, Chien C-C, Tzeng D-S, Lung F-W. Purple urine bag syndrome in nursing homes: Ten elderly case reports and a literature review. Clinical Interventions in Aging. 2008;3(4):729-734.
A dry and often bothersome cough is the most common adverse effect of ACE inhibitors. Recent studies indicate that cough may develop in ~10% of the patients treated with ACE inhibitors.
WHY? Mechanism unknown. It is thought to likely involve the protussive mediators: 1) bradykinin and 2) substance P. Normally they would be degraded by ACE and when using ACEi they accumulate in the lungs causing a cough.