January 20, 2023. Olivia and Janelli explain that caffeine intake during pregnancy may cause short height in babies, and Anthony discusses the definition, evaluation, and management of AKI with Dr. Kooner.
January 20, 2023. Olivia and Janelli explain that caffeine intake during pregnancy may cause short height in babies, and Anthony discusses the definition, evaluation, and management of AKI with Dr. Kooner.
Introduction: Caffeine consumption during pregnancy.
Written by Olivia Weller, MS3, American University of the Caribbean School of Medicine; and Janelli Mendoza, MS3, Ross University School of Medicine.
Current Guidelines about caffeine during pregnancy: The American College of Obstetricians and Gynecologists (ACOG) current recommendations are to limit caffeine consumption during pregnancy to 200 mg of caffeine per day. Anything exceeding a moderate level of caffeine intake has been linked to an increased risk for preterm birth and miscarriage. [8 oz of brewed coffee has approximately 137mg of caffeine. Other drinks and foods contain caffeine: Brewed tea 48mg; Decaf coffee (12 oz), 9-15 mg; caffeinated soft drink (12 oz) 37mg, Dark chocolate (1.45 oz) 30mg]
New Evidence: More recent data disclosed that moderate levels of caffeine consumed during pregnancy led to newborns being small for gestation age (SGA). This information was taken further, and scientists began to monitor these children as they aged. Researchers studied newborns born to mothers who consumed zero caffeine during pregnancy versus women who consumed moderate levels of caffeine. They tracked height, weight, BMI, and obesity risk but only found statistical differences in height. So far, they have only investigated children up to the age of 8 and found that the variance in height increased as the children got older. Therefore, even consuming a moderate level of caffeine during pregnancy can have lasting effects on a child’s height, which likely persists into adulthood. Some professionals are now saying there may be no amount of caffeine that is safe to consume during pregnancy.
American Family Physician Journal, 2009: “Caffeine intake is directly correlated with small but notable fetal growth restriction. Although a safe threshold cannot be determined, maternal caffeine intake of less than 100 mg per day minimizes the risk of fetal growth restriction.”
Why does smaller birth size matter? Caffeine crosses the placenta and acts as a vasoconstrictor which reduces the blood supply to the fetus and thus hinders proper growth. It is a sympathomimetic agent that can affect fetal stress hormones and increase the risk for rapid weight gain after birth. Although height is not a pressing issue, children are potentially more susceptible to increased risk for certain conditions later in life, such as obesity, heart disease, and diabetes. More research is needed on this front to make the conclusion that these differences do in fact persist into adulthood and lead to adverse health outcomes.
Conclusions and limitations. Pregnant women and children remain as a group with the least amount of research due to the potential adverse life outcomes. For this reason, the studies that have been done on caffeine consumption during pregnancy are comprised of self-reported data. Due to the association between high caffeine consumption and smoking, it is difficult to distinguish the two. Therefore, there is no clear cause-and-effect relationship between caffeine and intrauterine growth restriction (IUGR), leading to shorter stature later in life. However, the potential adverse health outcomes outweigh the psychological benefits of caffeine during the gestational period. If mothers can give up alcohol, drugs, smoking, raw fish, and so much more during pregnancy, why not caffeine too? With the emergence of this new information, perhaps it is time for a review of those guidelines.
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January 20, 2023. Written by Anthony Floresca, MS4, American University of the Caribbean School of Medicine; edited by Hector Arreaza, MD; recording done with Gagan Kooner, MD.
Definition of Acute Kidney Injury (AKI):
Acute kidney injury is a clinically relevant disease process that often occurs during hospitalizations but can also occur as a result of pre-existing diseases such as diabetes mellitus, hypertension, and congestive heart failure, usually referred to as “AKI on CKD,” i.e., acute kidney injury can present as a worsening of renal function in a patient who already has decreased renal function at baseline.
AKI is defined as a sudden onset decrease in renal function that can be diagnosed as early as 6 hours from disease onset. To diagnose AKI, specific parameters to consider are creatinine and urine output. Kidney Disease: Improving Global Outcomes or KDIGO established criteria in 2012 for diagnosing AKI:
Classification:
The severity of AKI is defined under the 2012 KDIGO guidelines:
Stage I
Stage II
Stage III
(Kooner: For example, if a creatinine at baseline is 0.8 and it increases to 2.4, it is stage III)
Anthony: Yes, it is stage III if the patient initiates renal replacement therapy (hemodialysis), OR a decrease in GFR to < 35 mL/min per 1.73 m^2 in patients <18 years old
The etiologies of AKI can be divided into three simplified categories:
Prerenal
Approximately 70% of cases of AKI are due to prerenal causes. This is due to a decrease in intravascular volume which in turn results in decreased renal perfusion. Medications such as ACE inhibitors and NSAID’s are selective vasoconstrictors that essentially decrease the amount of intravascular fluid that enters the kidney. Other causes include decreased perfusion as a result of loss of intravascular fluid such as hemorrhage.
The pathophysiology of prerenal AKI can be attributed to the renin-angiotensin-aldosterone system (RAAS). RAAS is activated in response to decreased intravascular volume. When intravascular volume is low, renin is secreted by juxtaglomerular cells in the afferent arterioles of the kidney. Renin activates angiotensin I which is converted to angiotensin II in the lungs. Angiotensin II directly activates aldosterone. The most detrimental effect of aldosterone on the kidneys is the vasoconstricting effect it has on the efferent arterioles which in turn decreases renal function.
Intrarenal
Intrarenal causes of AKI are largely due to direct renal damage either due to glomerular or tubular disease. Acute tubular necrosis (ATN) is an example of intrarenal AKI which can be caused by nephrotoxic agents such as certain antibiotics. ATN can also result from prolonged ischemia as a result of prerenal disease. Rhabdomyolysis can result in a large amount of myoglobin released into the blood which ends up being excreted by the kidney and causing intrarenal damage.
Contrast, given prior to imaging studies, is a radioactive compound that is excreted by the kidneys and can cause damage. This is why it is important to know a patient’s renal function prior to ordering studies with contrast. Most often, some proteins and drugs affect tubular cells and reduce their ability to function properly.
The pathophysiology for intrarenal causes of AKI is variable due to the different mechanisms by which diseases like systemic lupus erythematosus or Goodpasture syndrome lead to nephropathies.
Postrenal
Postrenal causes are largely structural abnormalities resulting in a subsequent decrease in renal excretion due to obstruction distal to the kidney. Examples are BPH, bladder/ prostate/ cervical cancer, or nephrolithiasis.
Management:
Most often the physical exam, history, and imaging studies can assist with diagnosing and treating this type of AKI. A patient with a history of fever and weight loss may suggest a diagnosis of cancer. A patient complaining of flank pain and dysuria may have stones that can be managed with lithotripsy.
Interestingly, a patient with unilateral obstruction may not necessarily develop an AKI as a single kidney can compensate for the affected kidney. The most common cause of postrenal AKI is bladder outlet obstruction due to bladder cancer, bladder stones, or tumors producing a mass effect. This results in bilateral kidney obstruction without adequate compensation. In this scenario, AKI is likely to develop.
Evaluation
Although AKI can manifest acutely, the recovery from AKI can take as long as months to years. Treating AKI is very much dependent on determining the cause.
For example, if a patient develops AKI following starting a new medication known to be nephrotoxic, it is important to stop the offending agent and consider adjusting the medication to renal dosing or consider alternative treatment options.
The most important method to determine the cause of AKI is fluid repletion. If a patient improves after receiving fluids, AKI is likely due to a prerenal etiology. AKI resulting from postrenal etiologies will likely improve following resolution or treatment of the distal obstruction. Otherwise, further tests and imaging can be useful in providing further information on the management of a patient with AKI.
Useful labs and imaging for the diagnosis and management of AKI:
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Conclusion: Now we conclude our episode number 126 “Caffeine and AKI.” We learned that caffeine intake, even below the recommended 200 mg, may cause an effect on newborns’ height. It may be time to review the guidelines for caffeine intake during pregnancy. Then, we listed to Anthony and Dr. Kooner’s explanation of Acute Kidney Injury. AKI presents when there is a serum creatinine increase of 0.3 mg/dL in 48 hours, or creatinine increase of 1.5 times from baseline, or decreased urine output below 0.5 mL/kg/h. If you keep in mind that definition, you will diagnose your patients in a timely manner to start kidney-saving treatments.
This week we thank Hector Arreaza, Olivia Weller, Janelli Mendoza, Anthony Floresca, and Gagan Kooner. Audio editing by Adrianne Silva.
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