These included genes (e.g., CLCN5, SLC34A1, SLC4A4, CLCNKA, and SLC12A1) implicated in Mendelian diseases where tubules fail to function, resulting in urinary wasting of electrolytes and low-molecular-weight proteins, together with acid-base aberrations. The gene discussed is SLC12A1; the disease is glycogen storage disease VI.