What links Urinary Oxalate and CKD Progression?

Are you aware of what a urinary oxalate excretion is? When one reaches high levels of oxalate, this can mean that the metabolite may be toxic. This can quickly become a problem because the metabolite is what’s eliminated through the kidney, thus the very fact that there may be high levels of oxalate has the potential to become harmful to anyone. Oxalate nephropathy is high concentration of oxalate in kidney tubular fluids which can create calcium oxalate crystals. This poses as a threat because these crystals can injure tubular epithelial cells

There are various types of disorders that may lead to the overproduction of oxalate such as hyperoxaluria. Disorders like hyperoxaluria can lead to an overproduction of oxalate which in turn can lead to end-stage renal disease or ESRD. While rare disorders may contribute to excess oxalate, there are many other channels that may also affect urinary oxalate excretion. This includes dietary oxalate intake, net intestinal absorption, and endogenous oxalate synthesis from the liver. This further proves that there may be reason to believe that there is a connection between high urinary oxalate levels and chronic kidney disease (CKD) as well as the loss of kidney function.

Additional factors that are associated with higher urinary oxalate excretion includes diabetes, lower eGFR, higher urine proteinuria, use of thiazide diuretics, lower serum calcium lower urinary calcium, high urine creatinine concentration, and even being a non-black race.

According to a study published by JAMA Internal Medicine, Dr. Waikar and colleagues studied the association between 24 hour urinary oxalate excretion and it’s interaction with the progression of CKD. This study was comprised of 3121 participant patients with moderate CKD. Of this sample pool, the median urinary oxalate excretion by 24-hour urine collection was 18.6mg in 24 hours with the interquartile range of 12.9-25.7 mg in 24 hours.

It should also be noted that the associations were consistent between the different subgroups based on demographics, level of kidney function, use of medications, and specific laboratory values. In addition to these notes, a second analysis proved that there were no associations between the urinary oxalate excretion and death. Moreover, the higher the levels of urinary oxalate excretion were, the greater the risk for kidney disease progression and ESRD was for patients with CKD. There were also findings that further proved that oxalate may be related to kidney damage. In one such case, there was a conclusion that calcium oxalate makes up 80% of kidney stones. Needless to say, most people often associate kidney stones with the increased risk for CKD.

From these studies, it can be concluded that calcium oxalate crystals can provoke and disturb the tubular lumen. Likewise, the deposition of the calcium oxalate may result in an inflammatory response. This can ultimately lead to stress and damage to the kidney.

Although the studies hold compelling evidence on oxalate and CKD, the interpretations should be reviewed with caution. This is due to the fact that the urinary oxalate levels were measured from frozen samples which can compromise the results. Since there are frozen and unfrozen samples, the reports may not be comparable. In addition to this difference, there are also interlaboratory variability in urinary oxalate measurements.

Yet, as aforementioned, the study does in fact provide compelling evidence that there is a risk factor for CKD progression and high levels of oxalate. Even if patients may not have nephrolithiasis, oxalate nephropathy may be a contributor to the loss of fundamental kidney functions. However, doctors recognize the need for more data in order to confidently determine whether interventions to reduce urinary oxalate excretions may be beneficial in regards to kidney functions.